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Background: Hepatocellular carcinoma (HCC) is the most common primary liver cancer and occurs frequently in patients with liver cirrhosis. HCC is the leading cause of cancer-related mortality around the globe. Aim: This study assessed the effects of thiamin in the anticancer activity of methotrexate (MTX) in diethyl nitrosamine (DEN) induced hepatocellular Carcinoma in Wistar strain male rats. Method: Fifty rats were randomly segregated in five groups with 10 rats in each group. HCC was induced by single intraperitoneal (i.p) dose of DEN (200 mg/kg) and HCC promoter phenobarbital was used in the basal diet (0.05%) for 5 days per week until the termination of the study in all the rats except for the normal control (NC) group. Disease control (DC) was given no treatment, while DM (DEN + MTX) and DT (DEN + thiamin) groups were given MTX (5 mg/kg, i.p per week for 16 weeks) and thiamin (25 mg/kg, orally, daily for 16 weeks), respectively. DMT (DEN + MTX + thiamin) group was given the combined dose of MTX and thiamin. Histopathological study was carried out to confirm the liver function tests such as α-feto protein (AFP), alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), total bilirubin (TB), and total protein (TP) along with antioxidants vascular endothelial growth factor (VEGF), lipid per-oxidation (LPO), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT). Results: Results showed that liver biomarkers and antioxidants parameters were still abnormal in the DC group while DM group showed significant restoration, but DT group showed less significant normalization. DMT showed mild recovery of these parameters. Conclusion: The mechanism of action of MTX and thiamin is antiparallel to each other and hence their concomitant administration may lead to inefficient anticancer activity of MTX. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the effect of coenzyme Q10 (CoQ10) on apoptotic myocardial cell death in rat model of heart ischemia and reperfusion I/R injury. Materials and Methods: Eighteen rats (200-250 g) were divided into three groups of 6 rats in each. Group I (sham-operated control group): this is the control group. The animals received the surgical procedure without IR injury or any drug treatment. Group II (I/R group): ischemia was accomplished by the occlusion of coronary artery for 30 min followed by reperfusion for 45 min and Group-III (Coenzyme Q10 treated group): Treated with CoQ10 at a dose of 1 mg/kg, postoperative for 7 days before induction of IR injury. Results: The study revealed that pretreatment with CoQ10 has shown protective effect on apoptotic rat heart and agreed with earlier reports that CoQ10 significantly protects from oxidative stress and cytopathological changes caused by cardiac ischemia followed by reperfusion and attenuated decrease of antioxidant enzymes. Nitric oxide production in the heart of ischemic rats was significantly increased by the pretreatment with CoQ10 in comparison with IR group. Conclusions: CoQ10 protects against cardiac apoptosis induced by IR injury by significantly decreasing the apoptotic DNA and regulating the expression of Bcl-2 gene. [ABSTRACT FROM AUTHOR]

Background: Osteoarthritis (OA) is a progressive joint disease characterized by gradual degradation of extracellular matrix (ECM) components in the cartilage and bone. The ECM of cartilage is a highly specified structure that is mainly composed of type II collagen and provides tensile strength to the tissue via aggrecan and proteoglycans. However, changes in the ECM composition and structure can lead to loss of collagen type II and network integrity. Several risk factors have been correlated with OA including age, genetic predisposition, hereditary factors, obesity, mechanical injuries, and joint trauma. Certain genetic association studies have identified several genes associated with OA using genome-wide association studies (GWASs). Results: We identified several novel genetic variants affecting genes that function in several candidate causative pathways including immune responses, inflammatory and cartilage degradation such as SELP, SPN, and COL6A6. Conclusions: The approach of whole-exome sequencing can be a promising method to identify genetic mutations that can influence the OA disease. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the protective effect of a novel polyherbal formulation against cisplatin‐induced hepatorenal toxicity in six groups of rats. Group I: Normal control; Group II: cisplatin (5 mg/kg i.p.); Group III: cisplatin (5 mg/kg i.p.) + cystone (750 mg/kg p.o.); Group IV: cisplatin + Costus speciosus, Fumaria indica, Cichorium intybus, and thymoquinone (CFCT) (25 mg/kg p.o.); Group V: cisplatin + CFCT‐50; Group VI: cisplatin + CFCT‐100. The rats were treated for 4 weeks. Serum and tissue biochemical parameters were assessed. The results showed that aspartate aminotransferase (131.8 IU/L), alanine aminotransferase (66.75 IU/L), alkaline phosphatase (168.67 IU/L), cholesterol (135.15 IU/L), serum urea (56.76 mg/dl), blood urea nitrogen (47.52 mg/dl), and creatinine (3.11 mg/dl) were significantly elevated (p <.001), while total protein (79.02 g/L) was reduced (p <.001) in the cisplatin group. These results were complemented by the outcomes of antioxidant parameters. Finally, CFCT formulation significantly ameliorated cisplatin toxicity. Practical applications: In this study, it is revealed that the administration of novel polyherbal formulation (Costus speciosus, Fumaria indica, Cichorium intybus, and thymoquinone [CFCT]) containing Costus speciosus, Fumaria indica, Cichorium intybus, and thymoquinone ameliorated cisplatin‐induced hepatorenal injury in rats. The ameliorative effects against cisplatin toxicity could be via contributing to the antioxidant defense system, by scavenging free radicals and reducing oxidative stress and inflammatory responses. This study aimed at being beneficial to cancer's patients, as they are compelled to take cisplatin, and ultimately suffer from the consequences of irreversible nephrotoxic damage. Furthermore, CFCT formulation could be considered as a dietary supplement for the reduction of cisplatin‐induced hepatorenal toxicity in cancer patients on cisplatin treatment. However, further clinical study is necessary. [ABSTRACT FROM AUTHOR]

Purpose: To synthesize and evaluate the antimicrobial activity of silver nanoparticles (AgNPs) derived from a supercritical carbon dioxide extract of the fresh aerial parts of Phyllanthus niruri. Methods: The synthesis of AgNPs of a P. niruri extract was carried out in a microwave oven. The extraction was carried out using a supercritical fluid extractor. The AgNPs were characterized by the Ultraviolet-visible (UV-vis) spectral analysis, Dynamic Light Scattering (DLS) zetasizer analysis, Transmission electron microscopy (TEM), X-ray diffraction (XRD) analysis and Fourier transform infrared (FT-IR) spectroscopy. The antimicrobial assays of AgNPs were carried out against different bacterial and fungal strains. Results: Results of various analytical techniques confirmed the synthesis of AgNPs of a P. niruri extract. The UV-vis spectroscopy showed an intense silver surface plasmon resonance band at 415 NM. The AgNPs had a mean size of 110 nm in the Zetasizer analysis. TEM images illustrated spherical AgNPs having a mean particle size of 110 nm. The X-ray diffractograms showed peaks at 38.17°, 44.28°, and 64.52°. The average crystallite size of Ag-NPs was found to be 110 nm. FT-IR spectra confirmed the stability of the AgNPs. The AgNPs demonstrated good antimicrobial effects against several tested pathogenic microbes. Conclusion: An efficiently synthesized AgNPs of P. niruri (SC-CO2) extract has been prepared by a simple, eco-friendly, cost-effective, rapid green chemistry methodology. The AgNPs of P. niruri extract possesses significant antimicrobial properties against the tested bacterial and fungal strains. [ABSTRACT FROM AUTHOR]

Background: Camel milk (CM) and Nigella sativa (NS) have been traditionally claimed to cure wide range of diseases and used as medicine in different part of world, particularly in Saudi Arabia. Several research studies have been published that proved beneficial effects of CM and NS., Objective: This study was undertaken to investigate the antihepatotxic potential of CM and NS oil (NSO) against thioacetamide (TAA)-induced hepato and nephrotoxicity in rats., Materials and Methods: Thirty female Albino Wistar rats were randomly divided in to six groups having five rats in each group. A single subcutaneous injection of TAA (100 mg/kg b. w.) was administered to all the rats in Group-II to VI on 1 st day to induce hepatorenal damage. Group I served as a normal control while Group II served as toxic control for comparison purpose. Experimental animals in Group III, IV, and V were supplemented with fresh CM, (250 mL/24 h/cage), NSO (2 mL/kg/day p. o.), and NSO + fresh CM, respectively. Group VI was treated with a polyherbal hepatoprotective Unani medicine Jigreen (2 mL/kg/day p. o.) for 21 days. TAA-induced hepatorenal damage and protective effects of CM and NSO were assessed by analyzing liver and kidney function tests in the serum. Histopathology of liver and kidney tissues was also carried out to corroborate the findings of biochemical investigation., Results: The results indicated that the TAA intoxicated rats showed significant increase in the alanine transaminase, aspartate transaminase, gamma-glutamyl transpeptidase, alkaline phosphatase, lipid profile, urea, creatinine, uric acid, sodium, and potassium levels in serum. Treatment of rats with CM, NSO, and CM plus NSO combination and Jigreen significantly reversed the damage and brought down the serum biochemical parameters and lipid profile toward the normal levels. The histopathological studies also support the hepato and nephroprotective effects of CM and NSO., Conclusion: This study demonstrated the ameliorative effects of CM, NSO, and CM plus NSO combination against TAA-induced hepatorenal toxicity in rats., Summary: The antihepatotxic potential of Camel's Milk (CM) and Nigella sativa oil (NSO) against thioacetamide (TAA) induced hepatorenal toxicity was evaluated in ratsThe oral administration of fresh CM (250 mL/24h/cage), NSO (2 mL/kg/day) and NSO+fresh CM and Jigreen (2 mL/kg/day) for 21 days significantly decreased the hepatorenal toxicity as evidenced from analyzed biochemical parameters in serum and histopathological studies of liver and kidney tissuesThis study demonstrated the ameliorative effects of CM and NSO against TAA induced hepatorenal toxicity. Abbreviations used: CM: Camel milk; NS: Nigella sativa ; NSO: Nigella sativa Oil; TAA: Thioacetamide; S.C.: Subcutaneous; Jig: Jigreen; b.w.: Body Weight; mL: Milli liter; mg: Milli gram; g: Gram; Kg: Kilo gram; ALT: Alanine transaminase; AST: Aspartate transaminase; GGT: Gamma-Glutamyl Transpeptidase; ALP: Alkaline Phosphatase; TC: Total Cholesterol; HDL-C: High Density Lipoprotein Cholesterol; LDL-C: Low Density Lipoprotein Cholesterol; TG: Triglyceride; TB: Total bilirubin; K + : Potassium; Na + : Sodium; CCl 4 : Carbon Tetrachloride; °C: Degree Celsius; p.o.: Per Oral; RPM: Revolutions per minute; H&E: Hematoxylin and Eosin; SEM: Standard Error of Mean; ANOVA: The one-way analysis of variance., Competing Interests: There are no conflicts of interest.

Objectives: To investigate the effect of coenzyme Q10 (CoQ10) on apoptotic myocardial cell death in rat model of heart ischemia and reperfusion I/R injury., Materials and Methods: Eighteen rats (200-250 g) were divided into three groups of 6 rats in each. Group I (sham-operated control group): this is the control group. The animals received the surgical procedure without IR injury or any drug treatment. Group II (I/R group): ischemia was accomplished by the occlusion of coronary artery for 30 min followed by reperfusion for 45 min and Group-III (Coenzyme Q 10 treated group): Treated with CoQ 10 at a dose of 1 mg/kg, postoperative for 7 days before induction of IR injury., Results: The study revealed that pretreatment with CoQ 10 has shown protective effect on apoptotic rat heart and agreed with earlier reports that CoQ 10 significantly protects from oxidative stress and cytopathological changes caused by cardiac ischemia followed by reperfusion and attenuated decrease of antioxidant enzymes. Nitric oxide production in the heart of ischemic rats was significantly increased by the pretreatment with CoQ 10 in comparison with IR group., Conclusions: CoQ 10 protects against cardiac apoptosis induced by IR injury by significantly decreasing the apoptotic DNA and regulating the expression of Bcl-2 gene., Competing Interests: There are no conflicts of interest.