90 results on '"Jagdale, Pankaj"'
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2. 4-Methylbenzylidene camphor induced neurobehavioral toxicity in zebrafish (Danio rerio) embryos
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Prakash, Ved, Chauhan, Shweta Singh, Ansari, Mohammad Imran, Jagdale, Pankaj, Ayanur, Anjaneya, Parthasarathi, Ramakrishnan, and Anbumani, Sadasivam
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- 2024
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3. Rifampicin-induced ER stress and excessive cytoplasmic vacuolization instigate hepatotoxicity via alternate programmed cell death paraptosis in vitro and in vivo
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Kainat, KM, Ansari, Mohammad Imran, Bano, Nuzhat, Jagdale, Pankaj Ramji, Ayanur, Anjaneya, Kumar, Mahadeo, and Sharma, Pradeep Kumar
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- 2023
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4. Author Correction: Potential of Quercetin to Protect Cadmium Induced Cognitive Deficits in Rats by Modulating NMDA‑R Mediated Downstream Signaling and PI3K/AKT—Nrf2/ARE Signaling Pathways in Hippocampus
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Srivastava, Anugya, Kumari, Anima, Jagdale, Pankaj, Ayanur, Anjaneya, Pant, Aditya Bhushan, and Khanna, Vinay Kumar
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- 2023
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5. Safety studies of Nexrutine, bark extract of Phellodendron amurense through repeated oral exposure to rats for 28 days
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Alam, Shamshad, Mandal, Payal, Jagdale, Pankaj Ramji, Ayanur, Anjaneya, and Ansari, Kausar Mahmood
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- 2021
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6. Safety evaluation of Ochratoxin A and Citrinin after 28 days repeated dose oral exposure to Wistar rats
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Jagdale, Pankaj Ramji, Dev, Indra, Ayanur, Anjaneya, Singh, Dhirendra, Arshad, Md, and Ansari, Kausar Mahmood
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- 2020
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7. Accelerated and scarless wound repair by a multicomponent hydrogel through simultaneous activation of multiple pathways
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Bhattacharya, Dipsikha, Tiwari, Ratnakar, Bhatia, Tejasvi, Purohit, Mahaveer Prasad, Pal, Anu, Jagdale, Pankaj, Mudiam, Mohana Krishna Reddy, Chaudhari, Bhushan Pradosh, Shukla, Yogeshwar, Ansari, Kausar Mahmood, Kumar, Ashok, Kumar, Pradeep, Srivastava, Vikas, and Gupta, Kailash Chand
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- 2019
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8. Sub-acute oral exposure of zinc oxide nanoparticles causes alteration in iron homeostasis through acute phase response: A protective effect by surface modification
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Srivastav, Anurag Kumar, Dhiman, Nitesh, Tiwari, Ratnakar, Arjaria, Nidhi, Prakash, Jyoti, Jagdale, Pankaj, Ayanur, Anjaneya, Singh, Dhirendra, Patnaik, Satyakam, and Kumar, Mahadeo
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- 2019
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9. Chronic exposure to Zearalenone leads to endometrial hyperplasia in CD-1 mice by altering the inflammatory markers.
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Singh, Varsha, Mandal, Payal, Chauhan, Shweta Singh, Saifi, Ishrat Jahan, Marhaba, Sandeep, P V, Jagdale, Pankaj, Ayanur, Anjaneya, and Ansari, Kausar Mahmood
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ENDOMETRIAL hyperplasia ,INFLAMMATORY mediators ,BLOOD proteins ,ESTRADIOL ,END of treatment ,ENDOMETRIUM ,MICE - Abstract
Background Zearalenone (ZEA), a natural food contaminant, is reported to act as a mycoestrogen due to its estrogen-mimicking properties. According to studies, ZEA has a greater potential for estrogenic activity compared to any other naturally occurring non-steroidal estrogen. ZEA has been found in the endometrium of individuals with reproductive problems and the serum of children facing early puberty. These studies suggested a possible link between ZEA exposure and endometrial toxicity; nonetheless, no thorough research has been done. This study assessed the endometrium's response to chronic ZEA exposure. Methods Four groups of CD-1 female mice were exposed to control, estradiol (E2), and two different doses of ZEA for 90 days. At the end of treatment, blood and uterus were collected, and samples were used for inflammatory cytokines level, immunochemical, histopathological, and biophysical analysis. Results Our data indicated that the uterus showed a change in body/organ weight ratio, while other organs did not have any notable changes. Immunochemical and histological studies showed hyperplasia and a higher number of glands in the endometrium after ZEA and E2 exposure. Similarly, proliferation markers such as proliferative cell nuclear antigen (PCNA), Ki-67, and inflammatory cytokines such as interleukin 6 (IL-6), interleukin 8 (IL-8), and interferon-gamma (IFN-?) levels were found to be higher in the E2 and ZEA-exposed groups. Conclusion Our finding conclude that ZEA targets the uterus and cause inflammation due to increased levels of inflammatory cytokines and proliferation mediators, as well as systemic toxicity denoted by a strong binding affinity with serum proteins. [ABSTRACT FROM AUTHOR]
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- 2024
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10. Lambda-cyhalothrin enhances inflammation in nigrostriatal region in rats: Regulatory role of NF-κβ and JAK-STAT signaling
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Kumari, Anima, Srivastava, Anugya, Jagdale, Pankaj, Ayanur, Anjaneya, and Khanna, Vinay Kumar
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The risk to develop neurobehavioural abnormalities in humans on exposure to lambda-cyhalothrin (LCT) - a type II synthetic pyrethroid has enhanced significantly due to its extensive uses in agriculture, homes, veterinary practices and public health programs. Earlier, we found that the brain dopaminergic system is vulnerable to LCT and affects motor functions in rats. In continuation to this, the present study is focused to unravel the role of neuroinflammation in LCT-induced neurotoxicity in substantia nigra and corpus striatum in rats. Increase in the mRNA expression of proinflammatory cytokines (TNF- α, IL-1β, IL-6) and iNOS whereas decrease in anti-inflammatory cytokine (IL-10) was distinct both in substantia nigra and corpus striatum of rats treated with LCT (0.5, 1.0, 3.0 mg/kg body weight, p.o, for 45 days) as compared to control rats. Further, LCT-treated rats exhibited increased levels of glial fibrillary acidic protein (GFAP) and ionized calcium-binding adapter molecule 1 (Iba-1), the glial marker proteins both in substantia nigra and corpus striatum as compared to controls. Exposure of rats to LCT also caused alterations in the levels of heat shock protein 60 (HSP60) and mRNA expression of toll-like receptors (TLR2 and TLR4) in the substantia nigra and corpus striatum. An increase in the phosphorylation of key proteins involved in NF-kβ (P65, Iκβ, IKKα, IKKβ) and JAK/STAT (STAT1, STAT3) signaling and alteration in the protein levels of JAK1 and JAK2 was prominent in LCT-treated rats. Histological studies revealed damage of dopaminergic neurons and reactive gliosis as evidenced by the presence of darkly stained pyknotic neurons and decrease in Nissl substance and an increase in infiltration of immune cells both in substantia nigra and corpus striatum of LCT-treated rats. Presence of reactive microglia and astrocytes in LCT-treated rats was also distinct in ultrastructural studies. The results exhibit that LCT may damage dopaminergic neurons in the substantia nigra and corpus striatum by inducing inflammation as a result of stimulation of neuroglial cells involving activation of NF-κβ and JAK/STAT signaling.
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- 2023
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11. Corrigendum to “Lambda-cyhalothrin enhances inflammation in nigrostriatal region in rats: Regulatory role of NF-κβ and JAK-STAT signaling” [NeuroToxicology 96 (2023) 101–117]
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Kumari, Anima, Srivastava, Anugya, Jagdale, Pankaj, Ayanur, Anjaneya, and Khanna, Vinay Kumar
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- 2023
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12. Polymer-Assisted In Situ Synthesis of Silver Nanoparticles with Epigallocatechin Gallate (EGCG) Impregnated Wound Patch Potentiate Controlled Inflammatory Responses for Brisk Wound Healing
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Kar,Aditya K, Singh,Amrita, Dhiman,Nitesh, Purohit,Mahaveer P, Jagdale,Pankaj, Kamthan,Mohan, Singh,Dhirendra, Kumar,Mahadeo, Ghosh,Debabrata, Patnaik,Satyakam, Kar,Aditya K, Singh,Amrita, Dhiman,Nitesh, Purohit,Mahaveer P, Jagdale,Pankaj, Kamthan,Mohan, Singh,Dhirendra, Kumar,Mahadeo, Ghosh,Debabrata, and Patnaik,Satyakam
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Aditya K Kar,1,2 Amrita Singh,1,2 Nitesh Dhiman,1,2 Mahaveer P Purohit,1,2 Pankaj Jagdale,3 Mohan Kamthan,4 Dhirendra Singh,3 Mahadeo Kumar,3 Debabrata Ghosh,2,5 Satyakam Patnaik1,2 1Water Analysis Laboratory, Nanomaterial Toxicology Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow 226001, Uttar Pradesh, India; 2Academy of Scientific and Innovative Research (AcSIR), CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow 226001, Uttar Pradesh, India; 3Regulatory Toxicology, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow 226001, Uttar Pradesh, India; 4CITAR, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow 226001, Uttar Pradesh, India; 5Immunotoxicology Laboratory, Food Drug and Chemical Toxicology Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow 226001, Uttar Pradesh, IndiaCorrespondence: Satyakam PatnaikWater Analysis Laboratory, Nanomaterial Toxicology Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow 226001, Uttar Pradesh, IndiaTel +91 5222627586, Ext. 205Fax +91 5222628227Email satyakampatnaik@yahoo.comIntroduction: An ideal wound dressing material needs to be predisposed with desirable attributes like anti-infective effect, skin hydration balance, adequate porosity and elasticity, high mechanical strength, low wound surface adherence, and enhanced tissue regeneration capability. In this work, we have synthesized hydrogel-based wound patches having antibacterial silver nanoparticles and antioxidant epigallocatechin gallate (EGCG) and showed fast wound closure through their synergistic interaction without any inherent toxicity.Methods and results: Wound patches were synthesized from modified guar gum polymer and assessed to determine accelerated wound healing. The modified polymer beget chemical-free in-situ synthesis of monodispersed silver NPs (∼12 nm), an antimicrobial agent, besides lending io
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- 2019
13. Control Release of Adenosine Potentiate Osteogenic Differentiation within a Bone Integrative EGCG-g-NOCC/Collagen Composite Scaffold toward Guided Bone Regeneration in a Critical-Sized Calvarial Defect
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Verma, Neeraj K., Kar, Aditya K., Singh, Amrita, Jagdale, Pankaj, Satija, Neeraj K., Ghosh, Debabrata, and Patnaik, Satyakam
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The regeneration of critical-sized bone defects with biomimetic scaffolds remains clinically challenging due to avascular necrosis, chronic inflammation, and altered osteogenic activity. Two confounding mechanisms, efficacy manipulation, and temporal regulation dictate the scaffold’s bone regenerative ability. Equally critical is the priming of the mesenchymal stromal cells (MSCs) toward lineage-specific differentiation into bone-forming osteoblast, which particularly depends on varied mechanochemical and biological cues during bone tissue regeneration. This study sought to design and develop an optimized osteogenic scaffold, adenosine/epigallocatechin gallate-N,O-carboxymethyl chitosan/collagen type I (AD/EGCG-g-NOCC@clgn I), having osteoinductive components toward swift bone regeneration in a calvarial defect BALB/c mice model. The ex vivofindings distinctly establish the pro-osteogenic potential of adenosine and EGCG, stimulating MSCs toward osteoblast differentiation with significantly increased expression of alkaline phosphatase, calcium deposits, and enhanced osteocalcin expression. Moreover, the 3D matrix recapitulates extracellular matrix (ECM) properties, provides a favorable microenvironment, structural support against mechanical stress, and acts as a reservoir for sustained release of osteoinductive molecules for cell differentiation, proliferation, and migration during matrix osteointegration observed. Evidence from in vivoexperiments, micro-CT analyses, histology, and histomorphometry signify accelerated osteogenesis both qualitatively and quantitatively: effectual bone union with enhanced bone formation and new ossified tissue in 4 mm sized defects. Our results suggest that the optimized scaffold serves as an adjuvant to guide bone tissue regeneration in critical-sized calvarial defects with promising therapeutic efficacy.
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- 2021
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14. Polymer-Assisted In Situ Synthesis of Silver Nanoparticles with Epigallocatechin Gallate (EGCG) Impregnated Wound Patch Potentiate Controlled Inflammatory Responses for Brisk Wound Healing.
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Kar, Aditya K, Singh, Amrita, Dhiman, Nitesh, Purohit, Mahaveer P, Jagdale, Pankaj, Kamthan, Mohan, Singh, Dhirendra, Kumar, Mahadeo, Ghosh, Debabrata, and Patnaik, Satyakam
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- 2019
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15. Genotoxicity evaluation of zinc oxide nanoparticles in Swiss mice after oral administration using chromosomal aberration, micronuclei, semen analysis, and RAPD profile.
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Srivastav, Anurag Kumar, Kumar, Akhilesh, Prakash, Jyoti, Singh, Dhirendra, Jagdale, Pankaj, Shankar, Jai, and Kumar, Mahadeo
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GENETIC toxicology ,ZINC oxide ,NANOPARTICLES ,CHROMOSOME abnormalities ,NUCLEOLUS ,SEMEN analysis ,RAPD technique - Abstract
The expanded uses of zinc oxide nanoparticles (ZnO NPs) have grown rapidly in the field of nanotechnology. Thus, rising production of nanoparticles (NPs) increases the possible risks to the environment and occupationally exposed humans. Hence, it is indispensable to appraise the safety toxicity including genotoxicity for these NPs. In the present study, we have evaluated the genotoxic effect ofZnONPs after oral administration to Swissmice at dose levels of 300 and 2000 mg/kg body weight. These doses were administered for 2 days at 24 h apart. Chromosomal aberration (CA) and micronucleus tests were conducted following Organization for Economic Co-operation and Development guidelines. DNA damage was evaluated at 0, 24, 48, and 72 h posttreatment using a randomly amplified polymorphic DNA (RAPD) assay; additionally, semen analyses were also performed at 34.5 days post oral exposure. The reactive oxygen species (ROS), 8-oxo-20-deoxyguanosine andCAs were increased (p < 0.05) at the highest dosage (2000mg/kg) of ZnONPs compared to controls. Aberrant spermmorphology with reduced sperm count and motility were also present (p < 0.05) in the high-dose group. Based on the RAPD assay, the genomic template stability within the high-dose group (<90%) was less than the controls (100%). The results suggested that ZnO NPs are mildly genotoxic in a dose-related manner and this toxicity were induced by generation of ROS. [ABSTRACT FROM AUTHOR]
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- 2017
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16. The interesting facts about rodent (rat) unique eating behavior
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Jagdale, Pankaj and B H Manjunatha Prabhu
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- 2012
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17. Molecular markers (Microsatellites) for genetic monitoring of mice
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Jagdale, Pankaj, B H Manjunatha Prabhu, Negi, Hema, and Mahadeo Kumar
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- 2012
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18. A comprehensive toxicity study of zinc oxide nanoparticles versus their bulk in Wistar rats.
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Srivastav, Anurag Kumar, Kumar, Mahadeo, Ansari, Nasreen Ghazi, Jain, Abhishek Kumar, Shankar, Jai, Arjaria, Nidhi, Jagdale, Pankaj, and Singh, Dhirendra
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ZINC oxide ,METAL nanoparticles ,METAL toxicology ,LABORATORY rats ,HEMATOLOGY ,BIOCHEMISTRY ,URINALYSIS - Abstract
The purpose of this study was to characterize the zinc oxide nanoparticles (ZnO-NPs) and their bulk counterpart in suspensions and to access the impact of their acute oral toxicity at doses of 300 and 2000 mg/kg in healthy female Wistar rats. The hematological, biochemical, and urine parameters were accessed at 24 and 48 h and 14 days posttreatment. The histopathological evaluations of tissues were also performed. The distribution of zinc content in liver, kidney, spleen, plasma, and excretory materials (feces and urine) at 24 and 48 h and 14 days posttreatment were accessed after a single exposure at dose of 2000 mg/kg body weight. The elevated level of alanine amino transferase, alkaline phosphatase, lactate dehydrogenase, and creatinine were observed in ZnO-NPs at a dose of 2000 mg/kg at all time points. There was a decrease in iron levels in all the treated groups at 24 h posttreatment as compared to control groups but returned to their normal level at 14 days posttreatment. The hematological parameters red blood cells, hemoglobin, hematocrit, platelets, and haptoglobin were reduced at 48 h posttreatment at a dose of 2000 mg/kg ZnO-NPs and showed hemolytic condition. All the treated groups were comparable to control group at the end of 14 days posttreatment. The zinc concentration in the kidney, liver, plasma, feces, and urine showed a significant increase in both groups as compared to control. This study explained that ZnO-NPs produced more toxicological effect as compared to their bulk particles as evidenced through alteration in some hemato-biochemical parameters and with few histopathological lesions in liver and kidney tissues. [ABSTRACT FROM AUTHOR]
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- 2016
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19. Bilayer Cryogel Wound Dressing and Skin Regeneration Grafts for the Treatment of Acute Skin Wounds
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Priya, S. Geetha, Gupta, Ankur, Jain, Era, Sarkar, Joyita, Damania, Apeksha, Jagdale, Pankaj R., Chaudhari, Bhushan P., Gupta, Kailash C., and Kumar, Ashok
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In this study, the potential of cryogel bilayer wound dressing and skin regenerating graft for the treatment of surgically created full thickness wounds was evaluated. The top layer was composed of polyvinylpyrrolidone-iodine (PVP-I) cryogel and served as the antiseptic layer, while the bottom regenerative layer was made using gelatin cryogel. Both components of the bilayer showed typical features of a cryogel interconnected macropore network, rapid swelling, high water uptake capacity of about 90%. Both PVP and gelatin cryogel showed high tensile strength of 45 and 10 kPa, respectively. Gelatin cryogel sheets were essentially elastic and could be stretched without any visible deformation. The antiseptic PVP-I layer cryogel sheet showed sustained iodine release and suppressed microbial growth when tested with skin pathogens (zone of inhibition ∼2 cm for sheet of 0.9 cm diameter). The gelatin cryogel sheet degraded in vitro in weeks. The gelatin cryogel sheet supported cell infiltration, attachment, and proliferation of fibroblasts and keratinocytes. Microparticles loaded with bioactive molecules (mannose-6-phosphate and human fibrinogen) were also incorporated in the gelatin cryogel sheets for their role in enhancing skin regeneration and scar free wound healing. In vivo evaluation of healing capacity of the bilayer cryogel was checked in rabbits by creating full thickness wound defect (diameter 2 cm). Macroscopic and microscopic observation at regular time intervals for 4 weeks demonstrated better and faster skin regeneration in the wound treated with cryogel bilayer as compared to untreated defect and the repair was comparable to commercial skin regeneration scaffold Neuskin-F. Complete skin regeneration was observed after 4 weeks of implantation with no sign of inflammatory response. Defects implanted with cryogel having mannose-6-phosphate showed no scar formation, while the wound treated with bilayer incorporated with human fibrinogen microparticles showed early signs of skin regeneration; epidermis formation occurred at 2 weeks after implantation.
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- 2016
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20. Evaluation of Three-Dimensional Chitosan-Agarose-Gelatin Cryogel Scaffold for the Repair of Subchondral Cartilage Defects: An In VivoStudy in a Rabbit Model
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Gupta, Ankur, Bhat, Sumrita, Jagdale, Pankaj R., Chaudhari, Bhushan P., Lidgren, Lars, Gupta, Kailash C., and Kumar, Ashok
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In this study, the potential of a chitosan-agarose-gelatin (CAG) cryogel scaffold for the repair of subchondral cartilage defects was explored in female New Zealand white rabbits. Custom-made CAG cryogel scaffold was implanted in a surgically created subchondral defect (diameter of 4 mm, depth of 4 mm) in knee joint of rabbit. The repair of the subchondral defect was evaluated at regular time interval by both macroscopic as well as microscopic examinations. The gross evaluation of the scaffold-implanted site showed integration of the scaffold with the surrounding tissue. Scanning electron microscopy and histological staining of the remnants of implanted cryogel scaffold showed infiltration of the host cells. The repair of the subchondral defect along with well-integrated regenerated cartilage was confirmed by the histology analysis of the joint. Results showed significant cartilage regeneration by the fourth week until eighth week after implantation. Immunohistochemical analysis confirmed that regenerated tissue is hyaline cartilage and absence of hypertrophy marker was reported. In addition, the CAG scaffolds did not elicit any adverse immunological rejection as shown by hematological analysis. Enzyme-linked immunosorbent assay did not show any statistically significant change in the concentration of tumor necrosis factor-α in the serum, and remained in a nontoxic range. Rabbits with a surgically created defect but no scaffold did not show any cartilage regeneration throughout the experiment of 8 weeks. These results demonstrate that CAG cryogel scaffolds promote repair of an osteochondral defect at a load-bearing site in rabbits.
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- 2014
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21. Influence of Photo-initiator concentration on photoactivation of composites prepared with LTCC and silver powders for DLP based 3D printing and their characterization
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Joseph, Jesly, Kondhalkar, Jyoti, Jagdale, Pankaj, Gadde, Janardhan Rao, Hawaldar, Ranjit, Kashid, Ranjit, Giramkar, Vijaya, and Joseph, Shany
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DLP (Digital Light Processing) based 3D (three dimensional) printing had been a widely used additive manufacturing technique with its broad aspects in rapid prototyping, packaging, biomedical applications, PCB etc due to its high resolution and reliability. Since, drive for miniaturization in electronic industry had been increasing; the need of additive manufacturing becomes better and reliable solution for fabrication of electronic device. In this study, we attempt to adopt LTCC (Low Temperature co-fired ceramic) technology with DLP based additive manufacturing machine to reduce lead time, running cost and investment cost while increasing production volume to levels suited for SMEs. This work reports our 3D Printing trials with composites using LTCC/dielectric and silver powder. Initial trials using the commercially available resins showed residue after firing the package which indicates its unsuitability for electronic packaging applications. Hence, the new resin was formulated by varying the Photo-initiator 2,4,6 -trimethyl benzoyl diphenyl phosphine oxide (TPO) Concentration. Photoresist was prepared by mixing the Photo-initiator (1 to 3wt %), Surfactant (2.5wt %) and diacrylate based monomer (96.5 -94.5wt%) in planetary mixer and the composition was optimised. Curing parameters for the unloaded resin such as exposure time, Intensity etc were varied accordingly and optimised. The photoresist and the printed samples were analysed for their viscosity, optical inspection, NMR, FTIR. Printing trials were done by preparing composites with Dielectric (LTCC) and conducting material (Silver) using above prepared photopolymer in 50:50 ratio. Effect of variation in the exposure time and intensity on the loading of functional material for curing has also been studied. Printed patterns were then sintered at about 875°C with standard LTCC firing cycle. No residue was observed after the sintering cycle. Trials using composites with different material were also tried. Characterisation of these composites and printed packages are reported. For 50% loading of functional material shrinkage of about 29% was observed. Effect of solid loading on shrinkage of sintered sample were also studied and reported.
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- 2022
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22. Rohitukine inhibits in vitro adipogenesis arresting mitotic clonal expansion and improves dyslipidemia in vivo[S]
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Varshney, Salil, Shankar, Kripa, Beg, Muheeb, Balaramnavar, Vishal M., Mishra, Sunil Kumar, Jagdale, Pankaj, Srivastava, Shishir, Chhonker, Yashpal S., Lakshmi, Vijai, Chaudhari, Bhushan P., Bhatta, Rabi Shankar, Saxena, Anil Kumar, and Gaikwad, Anil Nilkanth
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We developed a common feature pharmacophore model using known antiadipogenic compounds (CFPMA). We identified rohitukine, a reported chromone anticancer alkaloid as a potential hit through in silico mapping of the in-house natural product library on CFPMA. Studies were designed to assess the antiadipogenic potential of rohitukine. Rohitukine was isolated from Dysoxylum binacteriferumHook. to ⬧95% purity. As predicted by CFPMA, rohitukine was indeed found to be an antiadipogenic molecule. Rohitukine inhibited lipid accumulation and adipogenic differentiation in a concentration- and exposure-time-dependent manner in 3T3-L1 and C3H10T1/2 cells. Rohitukine downregulated expression of PPARγ, CCAAT/enhancer binding protein α, adipocyte protein 2 (aP2), FAS, and glucose transporter 4. It also suppressed mRNA expression of LPL, sterol-regulatory element binding protein (SREBP) 1c, FAS, and aP2, the downstream targets of PPARγ. Rohitukine arrests cells in S phase during mitotic clonal expansion. Rohitukine was bioavailable, and 25.7% of orally administered compound reached systemic circulation. We evaluated the effect of rohitukine on dyslipidemia induced by high-fat diet in the hamster model. Rohitukine increased hepatic expression of liver X receptor α and decreased expression of SREBP-2 and associated targets. Rohitukine decreased hepatic and gonadal lipid accumulation and ameliorated dyslipidemia significantly. In summary, our strategy to identify a novel antiadipogenic molecule using CFPMA successfully resulted in identification of rohitukine, which confirmed antiadipogenic activity and also exhibited in vivo antidyslipidemic activity.
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- 2014
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23. Biopolymeric composite hydrogel loaded with silver NPs and epigallocatechin gallate (EGCG) effectively manages ROS for rapid wound healing in type II diabetic wounds.
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Kar, Aditya K., Singh, Amrita, Singh, Divya, Shraogi, Nikita, Verma, Rahul, Saji, Joel, Jagdale, Pankaj, Ghosh, Debabrata, and Patnaik, Satyakam
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WOUND healing , *EPIGALLOCATECHIN gallate , *MACROPOROUS polymers , *HYDROGELS , *WOUND care , *LABORATORY mice , *WOUNDS & injuries , *SILVER - Abstract
Delayed wound healing in patients having type-II diabetes mellitus (T2DM) often results in a high rate of amputation. We report an innovative Guar Gum-based macroporous hydrogel (HG) infused with an antibacterial agent (Ag NPs), and antioxidant, epigallocatechin gallate (EGCG) to address rapid wound healing and interestingly could inhibit the associated pathophysical bone infection in a high-fat-diet-induced T2DM C57BL/6 mice model. The HG-Ag-EGCG elicits scar-free wound healing in subcutaneous wounds and histopathological evidence confirmed HG-Ag-EGCG hydrogel patch elicits better wound healing through enhanced cell proliferation, mature connecting tissue fiber formation, minimum void spaces formation, and better re-epithelialization when compared with a market available hydrogel patch material (Luofucon®). Supportive of the in vivo outcomes, in vitro experiments delineated better-wound closure due to improved management of ROS by the HG-Ag-EGCG. Additionally, a favorable non-toxicity outcome assessed through both in vitro and in vivo conditions confirmed its potential applicability in clinical wound care management. [ABSTRACT FROM AUTHOR]
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- 2022
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24. COX-2/EP2-EP4/β-catenin signaling regulates patulin-induced intestinal cell proliferation and inflammation.
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Singh, Neha, Bansal, Megha, Pal, Saurabh, Alam, Shamshad, Jagdale, Pankaj, Ayanur, Anjaneya, and Ansari, Kausar Mahmood
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INFLAMMATION , *CATENINS , *CELLULAR signal transduction , *CELL proliferation , *MYCOTOXINS , *GLUTATHIONE ,PHYSIOLOGICAL effects of patulin - Abstract
Abstract Patulin (PAT), a mycotoxin, is a natural contaminant that is produced by certain species of Penicillium, Aspergillus and Byssochlamys. The major contamination of PAT is in apple and apple based products. PAT is known to cause glutathione depletion, oxidative DNA damage and cell proliferation. Recently, in vitro studies have indicated that PAT can also increase the intestinal epithelial permeability, modulate tight junctions and decrease transepithelial electrical resistance. Nonetheless, no previous study has evaluated the mechanisms responsible for PAT-induced intestinal toxicity or its relevance to the in vivo situation. Here, Wistar rats were orally treated with 100 μg/kg body weight (b.wt.) of PAT, either alone or along with 100 mg/kg b. wt. of celecoxib for 3 days. We found that PAT exposure led to significantly higher levels of PGE 2 in serum and intestinal tissue and high expression of COX-2 and Ki-67 compared to controls. Interestingly, our results showed that celecoxib treatment could decrease the PAT-induced PGE 2 and reduce the PAT-induced intestinal damage. To study the mechanistic aspect, normal rat intestinal epithelial cells (IEC-6) were treated with non-toxic concentrations (100 nM, 250 nM and 500 nM) of PAT for 6 h. It was observed that PAT exposure caused enhanced proliferation, higher expression of COX-2, and EP2 and EP4 receptors, along with increased PGE 2 secretion. Additionally, PAT exposure caused enhanced Akt expression, which in turn inhibits GSK-3β and stabilizes β-catenin. Overall, our study suggests that the COX-2/EP2-EP4/β-catenin signaling cascades are involved in the regulation of PAT-induced intestinal cell proliferation and inflammation. Graphical abstract Unlabelled Image Highlights • Patulin exposure causes intestinal cell proliferation and inflammation. • Patulin causes over-expression of COX-2 and PGE 2 secretion. • EP2 and EP4 receptors are involved in the induction of COX-2 and PGE 2 secretion. • PGE 2 /EP2-EP4/β-catenin signaling regulates patulin induced intestinal toxicity. [ABSTRACT FROM AUTHOR]
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- 2018
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25. A clerodane diterpene inhibit adipogenesis by cell cycle arrest and ameliorate obesity in C57BL/6 mice.
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Beg, Muheeb, Shankar, Kripa, Varshney, Salil, Rajan, Sujith, Singh, Suriya Pratap, Jagdale, Pankaj, Puri, Anju, Chaudhari, Bhushan P., Sashidhara, Koneni V., and Gaikwad, Anil Nilkanth
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OBESITY genetics , *CLERODANES , *ADIPOGENESIS , *CELL cycle , *HYDROXYMETHYLGLUTARYL coenzyme A reductases , *GENE expression , *LABORATORY mice - Abstract
A clerodane diterpene, 16 α -Hydroxycleroda-3, 13 (14) Z-dien-15, 16-olide (compound 1 ) isolated from Polyalthia longifolia had previously been reported as a new structural class of HMG-CoA reductase inhibitor apart from statins. Statins are known to be anti-adipogenic in nature. The distant structural similarity between compound 1 and lovastatin (polyketide class of compound) prompted us to investigate effects of diterpene compound 1 on adipogenesis and thereby obesity. High content microscopy proved diterpene compound 1 exhibits better anti-adipogenic activity and less toxicity in differentiating adipocytes. Moreover, it reduced expression levels of PPARγ, C/EBPα and GLUT4 during differentiation in a time and concentration dependent manner. Diterpene compound 1 during early differentiation reduced MDI induced-Akt/mTOR phosphorylation and expression of cell cycle proteins, and thereby halted mitotic clonal expansion, the decisive factor in early adipogenesis. Further, its anti-adipogenic activity was validated in murine mesenchymal cell-line C3H10T1/2 and human mesenchymal stem cell models of adipogenic differentiation. When compound 1 was administered along with HFD, for another 8 weeks in 2 month HFD fed overweight mice (with BMI > 30 and impaired glucose tolerance), it attenuated weight gain and epididymal fat accumulation. It improved body glucose tolerance, reduced HFD induced increase in total cholesterol and leptin/adiponectin ratio. All these effects were comparable with standard anti-obesity drug Orlistat with added edge of potently decreasing circulating triglyceride levels comparable with normal chow fed group. Histological analysis shows that compound 1 inhibit adipocyte hypertrophy and decreased steatosis in hepatocytes. Both in vivo and in vitro results demonstrate a potential value of compound 1 as a novel anti-adipogenic and anti-obesity agent. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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26. A study on bisphenol S induced nephrotoxicity and assessment of altered downstream kidney metabolites using gas chromatography–mass spectrometry based metabolomics.
- Author
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Mandrah, Kapil, Jain, Veena, Shukla, Shagun, Ansari, Jamal Ahmad, Jagdale, Pankaj, Ayanur, Anjaneya, Srivastava, Vikas, and Roy, Somendu Kumar
- Subjects
- *
GAS chromatography/Mass spectrometry (GC-MS) , *NEPHROTOXICOLOGY , *KIDNEYS , *METABOLOMICS , *METABOLITES , *LIQUID chromatography-mass spectrometry , *POISONS - Abstract
The global use of bisphenol S (BPS) has now been significantly increased for commensurate utilization as a substitute for BPA for its regulatory concerns. Though, previous reports indicated that BPS been also appeared as a toxic congener comparable to BPA. In the present study, we determined nephrotoxicity condition induced due to BPS exposure. Results indicated that BPS significantly promoted histopathological disturbance in the kidney, and altered the levels of biomarkers of kidney damage in serum and urine samples of Wistar rats. It is also indicated that BPS altered the expression of kidney damage biomarkers associated with glomerular and tubular injury. Additionally, we determined the perturbation of kidney metabolites in the underlying pathophysiological response of kidney injury due to BPS exposure. Gas chromatography–mass spectrometry based untargeted metabolomics exhibited 20 significantly perturbed metabolites. Moreover, metabolic pathway analysis revealed significant disturbance in the TCA cycle and pyruvate metabolism pathways. • In vivo assessment was done to examine BPS induced nephrotoxicity. • BPS exposure shown histological changes in kidney of rats in dose depended manner. • Levels of kidney damage markers in serum and urine samples were found altered. • BPS exposure significantly perturbed metabolomic profile in kidney. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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27. TGF-β/Smad signaling pathway plays a crucial role in patulin-induced pro-fibrotic changes in rat kidney via modulation of slug and snail expression.
- Author
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Pal, Saurabh, Singh, Neha, Dev, Indra, Sharma, Vineeta, Jagdale, Pankaj Ramji, Ayanur, Anjaneya, and Ansari, Kausar Mahmood
- Subjects
- *
TRANSFORMING growth factors-beta , *VASCULAR endothelial growth factors , *MITOGEN-activated protein kinases , *CELLULAR signal transduction , *KIDNEY tubules - Abstract
Patulin (PAT) is a mycotoxin that contaminates a variety of food and foodstuffs. Earlier in vitro and in vivo findings have indicated that kidney is one of the target organs for PAT-induced toxicity. However, no study has evaluated the chronic effects of PAT exposure at environmentally relevant doses or elucidated the detailed mechanism(s) involved. Here, using in vitro and in vivo experimental approaches, we delineated the mechanism/s involved in pro-fibrotic changes in the kidney after low-dose chronic exposure to PAT. We found that non-toxic concentrations (50 nM and 100 nM) of PAT to normal rat kidney cells (NRK52E) caused a higher generation of reactive oxygen species (ROS) (mainly hydroxyl (•OH), peroxynitrite (ONOO−), and hypochlorite radical (ClO−). PAT exposure caused the activation of mitogen-activated protein kinases (MAPKs) and its downstream c-Jun/Fos signaling pathways. Moreover, our chromatin immunoprecipitation (ChIP) analysis suggested that c-Jun/Fos binds to the promoter region of Transforming growth factor beta (TGF-β 1) and possibly induces its expression. Results showed that PAT-induced TGF-β 1 further activates the TGF-β 1 /smad signaling pathways. Higher activation of slug and snail transcription factors further modulates the regulation of pro-fibrotic molecules. Similarly , in vivo results showed that PAT exposure to rats through gavage at 25 and 100 μg/kg b. wt had higher levels of kidney injury/toxicity markers namely vascular endothelial growth factor (VEGF), kidney Injury Molecule-1 (Kim-1), tissue inhibitor of metalloproteinase-1 (Timp-1), and clusterin (CLU). Additionally, histopathological analysis indicated significant alterations in renal tubules and glomeruli along with collagen deposition in PAT-treated rat kidneys. Overall, our data provide evidence of the involvement of ROS mediated MAPKs and TGF-β 1 /smad pathways in PAT-induced pro-fibrotic changes in the kidney via modulation of slug and snail expression. [Display omitted] • Low-dose chronic exposure to PAT caused pro-fibrotic changes in rat kidney. • Non-toxic concentrations of PAT caused activation of MAPKs and c-jun/c-fos. • Pharmacological inhibitor of JNK reduced the PAT-induced TGF-β expression. • Pharmacological inhibitor of TGF-β inhibited the PAT-induced EMT markers. • TGF-β/Smad pathway regulate pro-fibrotic changes via slug and snail expression. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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28. Prenatal arsenic exposure induces immunometabolic alteration and renal injury in rats.
- Author
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Singh RD, Tiwari R, Sharma V, Khan H, Gangopadhyay S, Singh S, Koshta K, Shukla S, Arjaria N, Mandrah K, Jagdale PR, Patnaik S, Roy SK, Singh D, Giri AK, and Srivastava V
- Abstract
Arsenic (As) exposure is progressively associated with chronic kidney disease (CKD), a leading public health concern present worldwide. The adverse effect of As exposure on the kidneys of people living in As endemic areas have not been extensively studied. Furthermore, the impact of only prenatal exposure to As on the progression of CKD also has not been fully characterized. In the present study, we examined the effect of prenatal exposure to low doses of As 0.04 and 0.4 mg/kg body weight (0.04 and 0.4 ppm, respectively) on the progression of CKD in male offspring using a Wistar rat model. Interestingly, only prenatal As exposure was sufficient to elevate the expression of profibrotic (TGF-β1) and proinflammatory (IL-1α, MIP-2α, RANTES, and TNF-α) cytokines at 2-day, 12- and 38-week time points in the exposed progeny. Further, alteration in adipogenic factors (ghrelin, leptin, and glucagon) was also observed in 12- and 38-week old male offspring prenatally exposed to As. An altered level of these factors coincides with impaired glucose metabolism and homeostasis accompanied by progressive kidney damage. We observed a significant increase in the deposition of extracellular matrix components and glomerular and tubular damage in the kidneys of 38-week-old male offspring prenatally exposed to As. Furthermore, the overexpression of TGF-β1 in kidneys corresponds with hypermethylation of the TGF-β1 gene-body, indicating a possible involvement of prenatal As exposure-driven epigenetic modulations of TGF-β1 expression. Our study provides evidence that prenatal As exposure to males can adversely affect the immunometabolism of offspring which can promote kidney damage later in life., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Singh, Tiwari, Sharma, Khan, Gangopadhyay, Singh, Koshta, Shukla, Arjaria, Mandrah, Jagdale, Patnaik, Roy, Singh, Giri and Srivastava.)
- Published
- 2023
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- View/download PDF
29. Arsenic exposure impels CD4 commitment in thymus and suppress T cell cytokine secretion by increasing regulatory T cells.
- Author
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Gera R, Singh V, Mitra S, Sharma AK, Singh A, Dasgupta A, Singh D, Kumar M, Jagdale P, Patnaik S, and Ghosh D
- Subjects
- Animals, Biomarkers, CD4-Positive T-Lymphocytes drug effects, CD4-Positive T-Lymphocytes immunology, CD4-Positive T-Lymphocytes metabolism, Cell Lineage, Core Binding Factor Alpha 3 Subunit genetics, Core Binding Factor Alpha 3 Subunit metabolism, Lymphocyte Count, Male, Mice, Spleen cytology, Spleen immunology, Spleen metabolism, T-Lymphocyte Subsets immunology, Thymocytes immunology, Transcription Factors genetics, Transcription Factors metabolism, Arsenic pharmacology, CD4 Antigens metabolism, Cytokines biosynthesis, T-Lymphocyte Subsets drug effects, T-Lymphocyte Subsets metabolism, T-Lymphocytes, Regulatory metabolism, Thymocytes drug effects, Thymocytes metabolism
- Abstract
Arsenic is globally infamous for inducing immunosuppression associated with prevalence of opportunistic infection in exposed population, although the mechanism remains elusive. In this study, we investigate the effect of arsenic exposure on thymocyte lineage commitment and the involvement of regulatory T cells (T
reg ) in arsenic-induced immunosuppression. Male Balb/c mice were exposed to 0.038, 0.38 and 3.8 ppm sodium arsenite for 7, 15 and 30 days through oral gavage. Arsenic exposure promoted CD4 lineage commitment in a dose dependent manner supported by the expression of ThPOK in thymus. Arsenic also increased splenic CD4+ T cells and promoted their differentiation into Treg cells. In parallel, arsenic exposure induced immunosuppression characterized by low cytokine secretion from splenocytes and increased susceptibility to Mycobacterium fortuitum (M. fortuitum) infection. Therefore, we linked arsenic-induced rise in Treg cells with suppressed Th 1 and Th 2 related cytokines, which has been reversed by inhibition of Treg cells in-vivo using wortmannin. Other parameters like body weight, kidney and liver function, histoanatomy of thymus and spleen as well as thymocyte and splenocytes viability were unaltered by arsenic exposure. Taken together our findings indicated that environmentally relevant dose of arsenic enhanced differentiation of Treg cells which in turn induce immunosuppression in experimental animals.- Published
- 2017
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30. Evaluation of three-dimensional chitosan-agarose-gelatin cryogel scaffold for the repair of subchondral cartilage defects: an in vivo study in a rabbit model.
- Author
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Gupta A, Bhat S, Jagdale PR, Chaudhari BP, Lidgren L, Gupta KC, and Kumar A
- Subjects
- Animals, Cartilage, Female, Microscopy, Electron, Scanning, Rabbits, Chitosan chemistry, Cryogels chemistry, Gelatin chemistry, Tissue Scaffolds chemistry
- Abstract
In this study, the potential of a chitosan-agarose-gelatin (CAG) cryogel scaffold for the repair of subchondral cartilage defects was explored in female New Zealand white rabbits. Custom-made CAG cryogel scaffold was implanted in a surgically created subchondral defect (diameter of 4 mm, depth of 4 mm) in knee joint of rabbit. The repair of the subchondral defect was evaluated at regular time interval by both macroscopic as well as microscopic examinations. The gross evaluation of the scaffold-implanted site showed integration of the scaffold with the surrounding tissue. Scanning electron microscopy and histological staining of the remnants of implanted cryogel scaffold showed infiltration of the host cells. The repair of the subchondral defect along with well-integrated regenerated cartilage was confirmed by the histology analysis of the joint. Results showed significant cartilage regeneration by the fourth week until eighth week after implantation. Immunohistochemical analysis confirmed that regenerated tissue is hyaline cartilage and absence of hypertrophy marker was reported. In addition, the CAG scaffolds did not elicit any adverse immunological rejection as shown by hematological analysis. Enzyme-linked immunosorbent assay did not show any statistically significant change in the concentration of tumor necrosis factor-α in the serum, and remained in a nontoxic range. Rabbits with a surgically created defect but no scaffold did not show any cartilage regeneration throughout the experiment of 8 weeks. These results demonstrate that CAG cryogel scaffolds promote repair of an osteochondral defect at a load-bearing site in rabbits.
- Published
- 2014
- Full Text
- View/download PDF
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