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Research in Pharmaceutical Sciences، جلد ۲۰، شماره ۱، صفحات ۰-۰
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عنوان انگلیسی Thymoquinone mitigates diclofenac-induced hepatorenal toxicity in male Wistar rats by balancing the redox state and modulating Bax/Bcl-2/caspase-3 apoptotic pathways and NF-κB signaling
چکیده انگلیسی مقاله Background and purpose: Diclofenac (DF), a widely used non-steroidal anti-inflammatory drug, can induce hepatotoxicity and nephrotoxicity. This study investigated the protective effects of thymoquinone (TQ), a bioactive compound from Nigella sativa , against DF-induced organ damage in rats. Experimental approach: Forty-eight male rats were divided into six groups (8 each) and treated orally for seven days as follows: group 1 (control): normal saline; group 2: DF (50 mg/kg); group 3: DF (50 mg/kg) + silymarin (50 mg/kg); groups 4-6: DF (50 mg/kg) + TQ at 10, 20, or 40 mg/kg, respectively. Serum biochemical parameters, hepatorenal oxidative stress markers, pro-inflammatory cytokines, and apoptosis-related genes were assessed. Histopathological examinations of liver and kidney tissues were also performed. Findings/Results: DF administration induced significant liver and kidney damage, evidenced by elevated serum biochemical markers, increased oxidative stress, inflammation, apoptosis-related gene expression, and histopathological alterations. TQ treatment, particularly at the highest dose (40 mg/kg) effectively attenuated these changes. TQ improved liver and kidney function, reduced oxidative stress markers, suppressed inflammation, modulated apoptosis-related gene expression, and ameliorated histopathological damage. Conclusion and implication: TQ exerted significant protective effects against DF-induced hepatorenal toxicity in rats, potentially through its antioxidant, anti-inflammatory, and anti-apoptotic properties. These findings suggest that TQ may be a promising therapeutic agent for mitigating DF-induced organ damage. However, further research, including clinical trials, is needed to confirm its efficacy and safety in humans.    
کلیدواژه‌های انگلیسی مقاله Apoptosis,Diclofenac,Hepatorenal toxicity,Inflammation,Oxidative stress,Thymoquinone.
نویسندگان مقاله | Amir Safi
Department of Biology, Faculty of Sciences, Urmia University, Urmia, Iran.


| Shakila Mohammadi
Department of Biology, Yazd University, Yazd, Iran.


| Mina Emami
Department of Life Sciences Engineering, Faculty of New Sciences and Technologies, University of Tehran, Tehran, Iran.


| Alireza Radaei
Department of Pathobiology, Faculty of Veterinary Science, Bu-Ali Sina University, Hamedan, Iran.


| Ali Kalantari-Hesari
Clinical Biochemistry Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.


| Ali Nouri
Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.


| Mohammad Rahimi-Madiseh
Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.


| Reza Ahmadi


نشانی اینترنتی http://rps.mui.ac.ir/index.php/jrps/article/view/2295
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نوع مقاله منتشر شده Original Article
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