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Extracellular matrix (ECM) scaffolds are extensively used in tissue engineering studies and numerous clinical applications for tissue and organ reconstructions. Due to the global severe shortage of human tissues and organs, xenogeneic biomaterials are a common source for human tissue engineering and regenerative medicine applications. Traditional methods for decellularization often disrupt the 3D architecture and damage the structural integrity of the ECM scaffold. To efficiently obtain natural ECM scaffolds from animal tissues and organs with intact architecture, we have developed a platform decellularization process using supercritical CO2 and tested its potential application in tissue engineering. A combination of human mesenchymal stem cells with a decellularized dermal matrix scaffold allowed complete regeneration of skin structure in a porcine full-thickness wound model.

Traditional purification of atelocollagen involves a harsh extraction process with environment-polluting chemicals and costly and/or time-consuming procedures which include salting-out, alkali, acid and enzymatic treatment and ion-exchange chromatography. The atelocollagen market is growing exponentially, with demand in the skincare industry and for various medical applications. As a result, there is an urgent need for an eco-friendly production process with minimal manipulation. We developed a novel technique involving supercritical carbon dioxide extraction technology to remove the cells and noncollagenous substances from the porcine hide. Subsequent processes allow the production of several products, including decellularized dermal membrane, high-purity collagen particles and atelocollagen. The advantages of our process are its faster speed and lower environmental impact and its generation of multiple products, including high purity atelocollagen with complete removal of telopeptides.

Damage to abdominal wall integrity occurs in accidents, infection and herniation. Repairing the hernia remains to be one of the most recurrent common surgical techniques. Supercritical carbon dioxide (SCCO2) was used to decellularize porcine skin to manufacture acellular dermal matrix (ADM) for the reparation of full-thickness abdominal wall defects and hernia. The ADM produced by SCCO2 is chemically equivalent and biocompatible with human skin. The ADM was characterized by hematoxylin and eosin (H&E) staining, 4,6-Diamidino-2-phenylindole, dihydrochloride (DAPI) staining, residual deoxyribonucleic acid (DNA) contents and alpha-galactosidase (α-gal staining), to ensure the complete decellularization of ADM. The ADM mechanical strength was tested following the repair of full-thickness abdominal wall defects (4 × 4 cm) created on the left and right sides in the anterior abdominal wall of New Zealand White rabbits. The ADM produced by SCCO2 technology revealed complete decellularization, as characterized by H&E, DAPI staining, DNA contents (average of 26.92 ng/mg) and α-gal staining. In addition, ADM exhibited excellent performance in the repair of full-thickness abdominal wall defects. Furthermore, the mechanical strength of the reconstructed abdominal wall after using ADM was significantly (p < 0.05) increased in suture retention strength (30.42 ± 1.23 N), tear strength (63.45 ± 7.64 N and 37.34 ± 11.72 N) and burst strength (153.92 ± 20.39 N) as compared to the suture retention (13.33 ± 5.05 N), tear strength (6.83 ± 0.40 N and 15.27 ± 3.46 N) and burst strength (71.77 ± 18.09 N) when the predicate device materials were concomitantly tested. However, the efficacy in hernia reconstruction of ADM is substantially equivalent to that of predicate material in both macroscopic and microscopic observations. To conclude, ADM manufactured by SCCO2 technology revealed good biocompatibility and excellent mechanical strength in post-repair of full-thickness abdominal wall defects in the rabbit hernia model. [ABSTRACT FROM AUTHOR]

About 30–50% of oral cancer patients require mandibulectomy and autologous fibula reconstruction. Autograft is the gold standard choice because of its histocompatibility; however, it requires additional surgery from the patient and with possible complications such as loss of fibula leading to calf weakening in the future. Allograft and xenograft are alternatives but are susceptible to immune response. Currently, no personalized bone xenografts are available in the market for large fascial bone defects. In addition, a large-sized complex shape bone graft cannot be produced directly from the raw material. We propose the use of porcine bones with 3D CAD/CAM carving to reconstruct a personalized, wide range and complex-shaped bone. We anticipate that patients can restore their native facial appearance after reconstruction surgery. Supercritical CO2 (SCCO2) technology was employed to remove the cells, fat and non-collagenous materials while maintaining a native collagen scaffold as a biomedical device for bone defects. We successfully developed 3D CAD/CAM carved bone matrices, followed by SCCO2 decellularization of those large-sized bones. A lock-and-key puzzle design was employed to fulfil a wide range of large and complex-shaped maxillofacial defects. To conclude, the 3D CAD/CAM carved bone matrices with lock and key puzzle Lego design were completely decellularized by SCCO2 extraction technology with intact natural collagen scaffold. In addition, the processed bone matrices were tested to show excellent cytocompatibility and mechanical stiffness. Thus, we can overcome the limitation of large size and complex shapes of xenograft availability. In addition, the 3D CAD/CAM carving process can provide personalized tailor-designed decellularized bone grafts for the native appearance for maxillofacial reconstruction surgery for oral cancer patients and trauma patients. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the efficacy of a novel decellularized porcine bone xenograft, produced by supercritical carbon dioxide extraction technology, on alveolar socket healing after tooth extraction compared to a commercially available deproteinized bovine bone (Bio‐Oss®). Materials and methods: Nine dogs (about 18 months old and weighing between 20 kg and 30 kg) underwent extractions of lower second to fourth premolars, bilaterally. The dogs were randomly selected and allocated to the following groups: Group 1: control unfilled socket; Group 2: socket filled with decellularized porcine bone xenograft (ABCcolla®) and covered by a commercially available porcine collagen membrane (Bio‐Gide®); Group 3: socket filled with Bio‐Oss® and covered by Bio‐Gide® membrane. One dogs from each group was sacrificed at 4‐, 12‐, and 24‐week to evaluate the socket healing after tooth extraction. The mandible bone blocks were processed without decalcification and specimens were embedded in methyl methacrylate and subjected to histopathology analyses to evaluate the bone regeneration in the extraction sockets. Results: At 24‐week after socket healing, ABCcolla® treated defects demonstrated significantly higher histopathology score in new bone formation and bone bridging, but significantly lower score in fluorescent labeling than those of the Bio‐Oss®. In the microphotographic examination, decellularized porcine bone xenograft showed similar characteristics of new bone formation to that of Bio‐Oss®. However, there was significantly less remnant implant materials in the decellularized porcine bone xenograft compared to the Bio‐Oss® group at 24‐week. Thus, the decellularized porcine bone graft seems to have promising bone regeneration properties similar to that of Bio‐Oss® with less remnant grafted material in a canine tooth extraction socket model. Conclusions: Within the limits of the study, we concluded that ABCcolla® treated defects demonstrated significantly more new bone formation and better bone bridging, but less amount of fluorescent labeling than those of the Bio‐Oss® group. However, clinical studies in humans are recommended to confirm these findings. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) including ulcerative colitis (UC) is one of the risk factors for the development of colitis-associated colon cancer (CAC). CAC is a type of colorectal cancer (CRC), the third leading cause of cancer death. Ziziphus jujuba (ZJ) fruit contains bioactive components such as polysaccharides, triterpenoid acid, and flavonoids, and it has shown anti-inflammatory property. The aim of the study was to investigate the protective effect of dietary ZJ on colitis-associated colorectal tumorigenesis in mice. Mice (n = 42, two sets) were injected with azoxymethane (AOM) followed by three cycles of 2% (w/v) dextran sulfate sodium (DSS) in drinking water to induce CAC. Simultaneously, those mice were fed with ZJ diet for 70 days (5% or 10% w/w). Data were analyzed by ANOVA followed by LSD Bonferroni test. Dietary ZJ decreased fecal blood, diarrhea, disease activity index (DAI), spleen weight (P < 0.001), and the number of tumors (P < 0.001). In addition, dietary ZJ increased colon length (P < 0.001) and suppressed the activation of NF-кB/IL-6/JAK1/STAT3 signaling pathway. In conclusion, we suggest that dietary ZJ attenuates inflammation by interfering NF-κB/IL-6/JAK1/STAT3 signaling pathway, thereby inhibits AOM/DSS-induced colon tumorigenesis in mice. [ABSTRACT FROM AUTHOR]

1. Chlorfenapyr [4-bromo-2-(4-chlorophenyl)-1-(ethoxymethl)-5-(trifluoromethyl)-1H-pyrrole-3-carbonitrile] is a commonly employed pesticide throughout the world. The mechanism of chlorfenapyr action is to uncouple oxidative phosphorylation in the mitochondria. The characteristic features of chlorfenapyr intoxication are high fever, rhabdomyolysis and neurologic symptoms that gradually get worse until death. 2. In recent years, suicide attempt cases using commercial chlorfenapyr pesticide were reported. Even small doses of commercial chlorfenapyr pesticide intoxication caused human fatality. However, world health organization (WHO) has classified chlorfenapyr as class 2-moderately hazardous chemical. Animal studies using technical grade (94.5%; AC 7504-59A) chlorfenapyr in 0.5% carboxy methyl cellulose as the vehicle, single dose through oral route in male rats were well tolerated. 3. We planned a therapeutic strategy for suicidal chlorfenapyr intoxication, therefore we evaluated the three different toxic doses of chlorfenapyr (10% chlorfenapyr and 90% detergent) through oral route in male rats for human extrapolation. The major difference between the technical grade chlorfenapyr and commercial grade chlorfenapyr was the vehicle. In the technical grade chlorfenapyr study, 0.5% carboxy methyl cellulose was used as a vehicle, whereas in the present study 90% detergent acted as a vehicle. The LD50 of commercial grade chlorfenapyr-40.63 mg/kg bw, which was approximately tenfold decrease than technical grade chlorfenapyr, LD50 – 441 mg/kg bw. 4. The combination of chlorfenapyr and detergent, a deadly cocktail to form micelle complex that can greatly influence bioavailability by attaching to biological membranesin vivo. To conclude, the enhanced bioavailability of chlorfenapyr by the detergent causes the fatality in suicidal attempts using chlorfenapyr. [ABSTRACT FROM PUBLISHER]

Sepsis is one of the major causes of death reported in intensive care units. Acute kidney injury (AKI) and hypotension are important in the pathogenesis and mortality of systemic inflammatory response (SIR). Sesamol delays mortality in sepsis; however, its effects on AKI and hypotension and the role of peroxisome proliferator-activated receptor-γ (PPAR-γ) activation have not been established. We investigated the effect of sesamol on SIR in cecal ligation and puncture (CLP)-induced acute kidney injury and lipopolysaccharide (LPS)-induced hypotension in rats. Sesamol was subcutaneously injected 1 h after SIR. Renal function (BUN and CRE) and proinflammatory mediators interleukin (IL)-1β and IL-6 were increased after CLP. Tumor necrosis factor (TNF)-α, IL-1β, IL-10, and nitrite production were significantly increased 6 h after LPS-induced hypotension (mean arterial pressure was significantly decreased). Sesamol significantly inhibited BUN, CRE, IL-1β, IL-6, and nitrite after CLP-induced acute renal injury. In addition, sesamol increased mean arterial pressure and IL-10, inhibited TNF-α and IL-1β, but did not affect nitrite production in LPS-induced hypotension. Sesamol increased PPAR-γ in the leucocytes and peritoneal macrophages in LPS-induced SIR. We conclude that sesamol regulates leucocyte and macrophage PPAR-γ-associated systemic cytokines expression, thereby ameliorates acute kidney injury and hypotension in rats. [ABSTRACT FROM AUTHOR]

Background. Allergic asthma is one of the most common chronic inflammatory diseases of airways. Severe asthma may lead to hospitalization and death. Sesame oil is a natural product with anti-inflammatory property. However, the effect of sesame oil on allergic asthma has never been studied. Objective. We investigate the effect of sesame oil on pulmonary inflammation in allergic asthma model. Methods. Allergic airway inflammation was induced by sensitizing with two doses of 10 mg ovalbumin (OVA) and then challenged with 1% OVA nebulizer exposure (1 h/day) for 3 days. Sesame oil (0.25, 0.5, or 1 mL/kg/day) was given orally 30 min before each challenge. Samples were collected 24 h after the last challenge. Results. Data showed that sesame oil inhibited pulmonary edema and decreased interleukin (IL)-1ß and IL-6 levels in bronchoalveolar lavage fluid in OVA-treated mice. Sesame oil also decreased pulmonary nitrite level, inducible nitric oxide synthase expression, and neutrophil infiltration induced by OVA. Further, sesame oil decreased serum IgE level in OVA-treated mice. Conclusion. Sesame oil may attenuate pulmonary edema and bronchial neutrophilic inflammation by inhibiting systemic IgE level in allergic asthma. [ABSTRACT FROM AUTHOR]

Stress-related mucosal disease (SRMD) causes considerable morbidity and mortality in critically ill patients. 3,4-Methylenedioxyphenol (sesamol) has been reported to have potent antioxidative and anti-inflammatory properties. The aim of this study was to investigate the effect of sesamol on water immersion restraint-(WIR-) induced SRMD in rats. Rat gastric ulcer and hemorrhage were induced by WIR. Rats were pretreated orally with various doses of sesamol (0.1, 0.3, and 1?mg/kg, resp.) 30?min before WIR. Gastric mucosal ulceration, hemoglobin, lipid peroxidation, mucus secretion, proinflammatory cytokines, and nuclear factor (NF)-κB levels were determined 4?h after WIR. In addition, the infiltration of neutrophil and macrophage into gastric mucosa was also determined after WIR. Water immersion restraint increased gastric mucosal ulcer and hemorrhage, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels but failed to affect mucosal lipid peroxidation and mucus secretion compared with non-WIR. Sesamol significantly decreased gastric ulceration and hemorrhage and inhibited mucosal TNF-α, IL-1β, and IL-6 production and NF-κB activity in WIR-treated rats. In addition, increased myeloperoxidase and CD68 levels in gastric mucosa were found in WIR-treated rats compared to non-WIR rats. Sesamol did not affect myeloperoxidase but decreased CD68 levels in mucosa in WIR-treated rats. Sesamol may protect against SRMD by inhibiting gastric mucosal proinflammatory cytokines in rats. [ABSTRACT FROM AUTHOR]

Background/Aims: The protective role of sesamol and its possible action against isoproterenol-induced myocardial injury and infarction is unknown. We tested the hypothesis that sesamol's protection against myocardial infarction is associated with the inhibition of matrix metalloproteinase (MMP)-2 and MMP-9. Methods: Four groups of experimental rats were subcutaneously injected with sesamol (0, 1, 3, or 10 mg/kg) and then, 2 h later, intraperitoneally injected with isoproterenol (100 mg/kg 24 h apart on 2 consecutive days) to induce myocardial infarction. Control rats were treated with saline only. Blood pressure (BP), heart rate (HR), and electrocardiography (ECG) wave durations, serum creatine phosphokinase isoenzymes (CKMB), lactate dehydrogenase (LDH), myocardial histology, MMP-2, and MMP-9 were assessed 24 h after the last dose of isoproterenol was given. Results: BP was lower, and HR, ECG wave durations, CKMB, LDH, myocardial injury, MMP-2, and MMP-9 levels were higher in experimental rats than in control rats. BP was significantly higher, and all the other parameters were significantly lower in the rats treated with sesamol than in those treated with isoproterenol only. Conclusions: Sesamol effectively prevented myocardial infarction, at least in part, by controlling proteolytic activities and the expression of MMP-2 and -9 in isoproterenol-treated rats. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background/Aims:We investigated the therapeutic effect of a single dose of sesame oil against gentamicin-induced renal damage in rats. Methods: Experimental rats were subcutaneously injected with gentamicin (100 mg/kg/day for 7 days) to induce renal injury. Sesame oil (1, 2 or 4 ml/kg) was given orally 24 h after the last dose of gentamicin. Control rats were treated with saline only. Renal injury, histopathological examination, histochemical staining, osteopontin expression, superoxide anion, nitric oxide, peroxynitrite radical and lipid peroxidation were assessed 24 h after sesame oil administration. Results: Serum blood urea nitrogen and creatinine as well as renal osteopontin expression, superoxide anion, nitric oxide, peroxynitrite radical and lipid peroxidation levels were higher in gentamicin-treated rats than in control rats. Sesame oil significantly decreased all the tested parameters compared with gentamicin-alone rats. Furthermore, histopathological and histochemical staining showed that renal tubules had recovered and regenerated in the sesame oil-treated rats. Conclusion: We hypothesize that a single dose of sesame oil inhibits oxidative stress to shorten the recovery period and allow the regeneration of renal tubules after the onset of gentamicin-induced renal injury in rats. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Large bone fractures with segmental defects are a vital phase to accelerate bone integration. The present study examined the role of supercritical carbon dioxide (scCO2) decellularized bone matrix (scDBM) seeded with allogeneic adipose-derived mesenchymal stem cells (ADSC) as bio-scaffold for bone regeneration. Bio-scaffold produced by seeding ADSC to scDBM was evaluated by scanning electron microscopy (SEM). Rat segmental femoral defect model was used as a non-union model to investigate the callus formation in vivo. Histological analysis and osteotomy gap closure in the defect area were analyzed at 12 and 24 weeks post-surgery. Immunohistochemical expression of Ki-67, BMP-2 and osteocalcin was evaluated to assess the ability of new bone formation scDBM. ADSC was found to attach firmly to scDBM bioscaffold as evidenced from SEM images in a dose-dependent manner. Callus formation was observed using X-ray bone imaging in the group with scDBM seeded with 2 × 106 and 5 × 106 ASCs group at the same time-periods. H&E staining revealed ASCs accelerated bone formation. IHC staining depicted the expression of Ki-67, BMP-2, and osteocalcin was elevated in scDBM seeded with 5 × 106 ASCs group at 12 weeks after surgery, relative to other experimental groups. To conclude, scDBM is an excellent scaffold that enhanced the attachment and recruitment of mesenchymal stem cells. scDBM seeded with ASCs accelerated new bone formation. [ABSTRACT FROM AUTHOR]

Stress-related mucosal disease (SRMD) causes considerable morbidity and mortality in critically ill patients. 3,4-Methylenedioxyphenol (sesamol) has been reported to have potent antioxidative and anti-inflammatory properties. The aim of this study was to investigate the effect of sesamol on water immersion restraint-(WIR-) induced SRMD in rats. Rat gastric ulcer and hemorrhage were induced by WIR. Rats were pretreated orally with various doses of sesamol (0.1, 0.3, and 1?mg/kg, resp.) 30?min before WIR. Gastric mucosal ulceration, hemoglobin, lipid peroxidation, mucus secretion, proinflammatory cytokines, and nuclear factor (NF)-κB levels were determined 4?h after WIR. In addition, the infiltration of neutrophil and macrophage into gastric mucosa was also determined after WIR. Water immersion restraint increased gastric mucosal ulcer and hemorrhage, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels but failed to affect mucosal lipid peroxidation and mucus secretion compared with non-WIR. Sesamol significantly decreased gastric ulceration and hemorrhage and inhibited mucosal TNF-α, IL-1β, and IL-6 production and NF-κB activity in WIR-treated rats. In addition, increased myeloperoxidase and CD68 levels in gastric mucosa were found in WIR-treated rats compared to non-WIR rats. Sesamol did not affect myeloperoxidase but decreased CD68 levels in mucosa in WIR-treated rats. Sesamol may protect against SRMD by inhibiting gastric mucosal proinflammatory cytokines in rats. [ABSTRACT FROM AUTHOR]

Background. Allergic asthma is one of the most common chronic inflammatory diseases of airways. Severe asthma may lead to hospitalization and death. Sesame oil is a natural product with anti-inflammatory property. However, the effect of sesame oil on allergic asthma has never been studied. Objective. We investigate the effect of sesame oil on pulmonary inflammation in allergic asthma model. Methods. Allergic airway inflammation was induced by sensitizing with two doses of 10 mg ovalbumin (OVA) and then challenged with 1% OVA nebulizer exposure (1 h/day) for 3 days. Sesame oil (0.25, 0.5, or 1 mL/kg/day) was given orally 30 min before each challenge. Samples were collected 24 h after the last challenge. Results. Data showed that sesame oil inhibited pulmonary edema and decreased interleukin (IL)-1ß and IL-6 levels in bronchoalveolar lavage fluid in OVA-treated mice. Sesame oil also decreased pulmonary nitrite level, inducible nitric oxide synthase expression, and neutrophil infiltration induced by OVA. Further, sesame oil decreased serum IgE level in OVA-treated mice. Conclusion. Sesame oil may attenuate pulmonary edema and bronchial neutrophilic inflammation by inhibiting systemic IgE level in allergic asthma. [ABSTRACT FROM AUTHOR]

Neuromorphic bioelectronics aim to integrate electronics with biological systems yet encounter challenges in biocompatibility, operating voltages, power consumption, and stability. This study presents biocompatible neuromorphic devices fabricated from acellular dermal matrix (ADM) derived from porcine dermis using low-temperature supercritical CO 2 extraction. The ADM preserves the natural scaffold structure of collagen and minimizes immunogenicity by eliminating cells, fats, and noncollagenous impurities, ensuring excellent biocompatibility. The ADM-based devices emulate biological ion channels with biphasic membrane current modulation, exhibiting temperature dependency and pH sensitivity. It operates at an ultralow voltage of 1 mV and demonstrates reliable synaptic modulation exceeding 4 × 10 4 endurance cycles. The activation voltage can be theoretically as low as 59 μV, comparable to brainwave signals with a power of merely 7 aJ/event. Furthermore, a brain-like forgetting visualization algorithm is developed, leveraging the synaptic forgetting plasticity of ADM-based devices to achieve complex computing tasks in a highly energy-efficient manner. Neuromorphic devices based on ADM not only hold potential in implantable biointerfaces due to their exceptional biocompatibility, ultralow voltage, and power but also provide a feasible way for energy-efficient computing paradigms through a synergistic hardware-software approach.

Bone defects can arise from numerous reasons, such as aging, tumor, trauma, infection, surgery, and congenital diseases. Bone grafts are commonly used as a substitute to fill the void and regenerate the defect. Due to its clean and green technology, the supercritical carbon dioxide (SCCO 2 ) extraction aided the production of bone grafts is a recent trend. The SCCO 2 -derived bone graft has osteoconductive and osteoinductive properties along with excellent biocompatible, nontoxic, bioabsorbable, osteoconductive, and good mechanical properties; however, clinical usage during surgery is time-consuming. Therefore, we produced a putty material combining bone graft powder and acellular dermal matrix (ADM) powder and tested its regenerative efficacy in the critical defect in the rabbit model. The putty was found to retain the tubular structure. In addition, the putty depicted excellent stickiness and cohesiveness in both saline and blood medium. The bone regeneration of bone graft and putty was similar; both had excellent bone healing and regeneration of critical defects as evaluated by the X-ray, microtomography, hematoxylin-eosin, Masson trichrome, and alizarin red staining. Putty contains a less washout rate, good mechanical strength, and biocompatibility. In conclusion, the SCCO 2 -derived moldable putty could be a promising easy-to-use alternative for bone grafts at present which might have real-world usage in orthopedics as a potential bone void filler and dental socket preservation., Competing Interests: We declare that we have no conflicts of interest.

At present, no definitive treatment for articular cartilage defects has been perfected. Most of the previous treatments involved multiple drilling and microfracture over defect sites with repair-related substances, which poses a limited therapeutic effect. End-stage therapy includes artificial knee joint replacement. In this study, we prepared a novel decellularized natural cartilage scaffold from porcine articular cartilage by supercritical CO 2 extraction technology and three-dimensional (3D) composites made using decellularized porcine cartilage graft (dPCG) as scaffolds, platelet-rich plasma (PRP), thrombin as signals and chondrocytes as cells for the treatment of articular cartilage defects. In this study, in vitro and in vivo cartilage regeneration and the expression of chondrogenic markers were examined. Decellularized cartilage graft (dPCG) was evaluated for the extent of cell and DNA removal. Residual cartilage ECM structure was confirmed to be type II collagen by SDS PAGE and immunostaining. The new 3D composite with dPCG (100 mg and 2 × 10 6 chondrocytes) scaffold promotes chondrogenic marker expression in vitro. We found that the in vivo 3D composite implanted cartilage defect showed significant regeneration relative to the blank and control implant. Immunohistochemical staining showed increase of expression including Collagen type II and aggrecan in 3D composite both in vitro and in vivo studies. In this study, the bioengineered 3D composite by combining dPCG scaffold, chondrocytes, and PRP facilitated the chondrogenic marker expression in both in vitro and in vivo models with accelerated cartilage regeneration. This might serve the purpose of clinical treatment of large focal articular cartilage defects in humans in the near future., (© 2020 John Wiley & Sons Ltd.)

Sleep deprivation affects all aspects of health. Adverse health effects by sleep deviation are still underestimated and undervalued in clinical practice and, to a much greater extent in monitoring human health. We hypothesized that sleep deprivation-induced mild organ injuries; oxidative stress and inflammation might play a crucial role in inducing multi-organ injury. Male C57BL/6J mice (n = 6-7) were sleep-deprived for 0-72 h using a modified multiple platform boxes method. Blood and tissue were collected. Liver, heart, kidney, lung, and pancreatic injuries were evaluated using biochemical and histological analyses. Glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), total billirubin (TBIL), creatine phosphokinase (CPK), creatine phosphokinase-myocardial band (CKMB), lactic dehydrogenase (LDH), creatinine (CRE), and blood urea nitrogen (BUN) were assayed in blood. Malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were measured. Histology revealed mild-to-moderate liver and lung injury in sleep-deprived mice. Sleep-deprived mice had significantly higher GOT, GPT, TBIL, CPK, CKMB, LDH, BUN, and α-amylase (AMYL) levels, which indicated liver, heart, kidney, and pancreatic injuries. Serum IL-1β at 24 h and IL-6 at 72 h were significantly higher in sleep-deprived than in control mice. Hepatic TNF-α and IL-1β were significantly higher, but IL-6 significantly lower in mice that had been sleep-deprived for 72 h. Sleep deprivation-mediated inflammation may be associated with mild to moderate multi-organ damage in mice. The implication of this study indicates sleep deprivation in humans may induce multi-organ injury that negatively affects cardiovascular and gastrointestinal health.

Ziziphus jujuba (ZJ) fruit is rich in bioactive functional components such as polysaccharides, triterpenoid acid, flavonoids and oleamide. It has been commonly used in the treatment of various diseases including diabetes, digestive disorders, diarrhea, skin infections, liver and urinary complaints. However, dietary effects with regard to chemoprevention of colon cancer have not been studied. The present study was performed to evaluate the protective effects of dietary ZJ against colitis-associated colon carcinogenesis in azoxymethane (AOM)-dextran sodium sulphate (DSS)-treated mice. AOM was injected (10 mg/kg b.wt., i.p.) and three cycles of 2% DSS in drinking water for 7 days with 14 days of normal drinking water in-between were administered to induce colitis-associated colon cancer. ZJ fruit was supplemented into feed at levels of 5 and 10%. Dietary ZJ significantly attenuated aberrant crypt foci (ACF) formation and also decreased the progression of hyperplasia to dysplasia. In addition, it significantly reduced circulating white blood cells, lymphocytes, neutrophils, monocytes, eosinophils, basophils and platelets compared to colon cancer mice. We conclude that ZJ supplementation may delay the progression of colon cancer from hyperplasia to dysplasia and ultimately adenocarcinoma and cancer. In addition, it decreased circulating tumor-related leukocytes, main regulators of cancer inflammation. Dietary consumption of ZJ fruit attenuated the formation of ACF and delayed the progression of colon cancer.

Background: Hypokalemia and hypertension are common manifestations of preclinical cardiovascular conditions that have a predictive value for cardiovascular morbidity and mortality. Cardiac hypertrophy, an important risk factor in heart failure, is attributed to long-term hypokalemia and hypertension. Sesame oil is rich in nutrients and possesses potent antihypertensive activities., Methods: We investigated the therapeutic potential of sesame oil using a hypertensive model created by subcutaneously injecting deoxycorticosterone acetate (DOCA; 15 mg/mL/kg in mineral oil; twice weekly for 5 weeks) and supplementing with 1% sodium chloride drinking water (DOCA/salt) to uninephrectomized rats. Sesame oil was administered by oral gavage (0.5 or 1 mL/kg/d for 7 days) after 4 weeks of DOCA/salt treatment. Systolic blood pressure (SBP) and diastolic blood pressure (DBP), electrocardiography (ECG), and K(+) and Mg(2+) levels were assessed 24 hours after the last dose of sesame oil. Heart tissue was collected for histologic analysis., Results: Sesame oil effectively reduced the SBP/DBP and ECG abnormalities and increased the serum levels of K(+) and Mg(2+) while limiting the urinary excretion of K(+) in DOCA/salt-induced hypertensive rats. In addition, sesame oil decreased the heart mass, the thickness of the left ventricle, and the diameter of cardiomyocytes, indicating the regression of left ventricular hypertrophy in the hypertensive rats., Conclusion: We demonstrate that sesame oil therapeutically ameliorates cardiac hypertrophy by regulating hypokalemia in hypertensive rats., (© 2013 American Society for Parenteral and Enteral Nutrition.)

Background: Sinusoidal obstruction syndrome (SOS) occurs in patients undergoing hematopoietic cell transplantation and chemotherapy. The chemotherapeutic drugs oxaliplatin and cyclophosphamide cause SOS. Sesame oil is a nutrient-rich antioxidant popular in alternative medicine. It contains sesamin, sesamol, and sesamolin, all of which contribute to its antioxidant property. The authors investigated the protective effect of prophylactic sesame oil against monocrotaline-induced SOS in rats., Methods: Male Sprague-Dawley rats were gavaged with a single dose of sesame oil (0.5, 1, 2, or 4 mL/kg). One hour later, those rats were gavaged with monocrotaline (90 mg/kg) to induce SOS. Control rats were treated with saline only. Aspartate transaminase, alanine transaminase, laminin, collagen, myeloperoxidase, nitrate content, lipid peroxidation, glutathione levels, matrix metalloproteinase (MMP)-9, and tissue inhibitor of matrix metalloproteinases (TIMP)-1 were assessed 48 hours after the monocrotaline gavage., Results: All tested parameters except TIMP-1, laminin, collagen, and glutathione were higher in monocrotaline-treated rats than in saline-only-treated control rats. In sesame oil-treated rats, all tested parameters except TIMP-1, laminin, collagen, and glutathione were significantly attenuated compared with monocrotaline-only-treated rats. Sesame oil downregulated MMP-9 expression but upregulated TIMP-1 expression in monocrotaline-only-treated rats. In addition, a histological analysis of liver tissue samples showed that sesame oil showed significant protection., Conclusion: A single prophylactic dose of sesame oil protects against SOS by downregulating MMP-9 expression, upregulating TIMP-1 expression, and inhibiting oxidative stress.

Background: The chemotherapeutic drug oxaliplatin causes sinusoidal obstruction syndrome (SOS), which is analogous to that of monocrotaline-induced SOS. Sesame oil is a nutrient-rich antioxidant in alternative medicine. It contains phenol, sesamin, sesamol, and sesamolin, all of which contribute to its antioxidant property. The authors investigated the therapeutic effect of oral sesame oil against monocrotaline-induced SOS in rats., Methods: Male Sprague-Dawley rats were gavaged with monocrotaline (90 mg/kg) to induce SOS. Control rats were treated with saline only at 0 and 24 hours. Sesame oil (0.5, 1, 2, or 4 mL/kg, orally) was given 24 hours after monocrotaline in rats. Blood samples were collected at 24 and 48 hours after monocrotaline was given to assess the level of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Histopathology was also assessed 48 hours after monocrotaline was given., Results: AST and ALT were significantly higher in monocrotaline-treated rats than in control rats. Oral sesame oil did not decrease AST and ALT in monocrotaline-treated rats. In addition, liver pathology revealed that oral sesame oil had no therapeutic effect against SOS., Conclusion: Oral sesame oil is therapeutically ineffectual against monocrotaline-induced SOS.

4-Nitroquinoline 1-oxide (4-NQO) a potent oral carcinogen, widely used for induction of oral carcinogenesis, has been found to induce lipid peroxidation in vivo and in vitro. Green tea contains a high content of polyphenols, which are potent antioxidants. Thus green tea polyphenols (GTP) might be expected play a protective role against 4-NQO induced lipid peroxidation and bone marrow toxicity. In the present study, a dose of 200 mg of GTP/kg b.wt/day was given orally for a week, simultaneously animals received 0.2 ml of 0.5% 4-NQO in propylene glycol (5 mg/ml) injected intramuscularly for three times/week. Oxidants and antioxidants such as malendialdehyde (MDA) and thiols, glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) were significantly decreased in 4-NQO induced animals except MDA, and these parameters were brought back to near normalcy on treatment with GTP. The results suggest that GTP treatment offers significant protection against 4-NQO induced lipid peroxidation and bone marrow toxicity and might be a promising potential candidate for prevention of mutations leading to cancer.

The aim of the study was to investigate the effect of sesame oil on acute kidney injury induced by the synergistic action of aminoglycoside and iodinated contrast in rats. Acute kidney injury was induced by a 5-day course of daily gentamicin injections (100 mg/kg of body weight, subcutaneously) and then iodinated contrast (4 ml/kg, intravenously) in male specific-pathogen-free Sprague-Dawley rats. Sesame oil (0.5 ml/kg, orally) was given 1 h before iodinated contrast. Renal function and oxidative stress were assessed 6 h after iodinated contrast injection. Renal function was evaluated by measuring serum blood urea nitrogen and creatinine levels. Renal oxidative stress was assessed by determining renal lipid peroxidation, myeloperoxidase, hydroxyl radical, superoxide anion, nitrite/nitrate, and inducible nitric oxide synthase levels. Sesame oil significantly prevented the rise of serum blood urea nitrogen and creatinine levels. Furthermore, there was a parallel inhibition of the rise in levels of expression of renal lipid peroxidation, myeloperoxidase, hydroxyl radicals, superoxide anion, nitrite/nitrate, and inducible nitric oxide synthase in rats with gentamicin-plus-iodinated contrast-induced acute kidney injury. We conclude that sesame oil may attenuate aminoglycoside-plus-iodinated contrast-induced acute kidney injury by inhibiting renal oxidative stress in rats.