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Articles by Ranjbar Akram
Total Records ( 2 ) for Ranjbar Akram
  Ranjbar Akram , Ghasemi Hassan , Hossini Zijoud Seyed-Mostafa , Mohsenzadeh Fariba , Chehregani Abdolkarim and Soleymanian Tayebeh
  Background and Objectives: Paraquat (PQ), one of the most widely used herbicides, is highly toxic to humans and animals. There is much information regarding its toxic effects on the lungs, but less is known about its toxicity in other organs. PQ is thought to play pivotal roles in the pathophysiology of acute renal failure and the progression of chronic kidney disease. The aim of this study was the effect of hydroalcoholic extract Matricaria chamomilla L. (M. chamomilla) against PQ-induced kidney injury in association with its antioxidant activity. Methodology: The male rats were treated with gavages’ daily with PQ (5 mg/kg/day) and M. chamomilla (50 mg/kg/day) were administered alone or in combination for 7 days. After treatments, blood urea nitrogen and creatinine levels, Total Antioxidant Capacity (TAC), total thiol molecules (TTG) levels and catalase CAT activity in kidney tissue were measured. Results: Rats administered PQ showed increased blood urea nitrogen and creatinine levels and CAT activity, TAC and TTG was decreased compared with control rats. Co-administration of PQ with M. chamomilla extract increased TAC and TTG in kidney tissue as compared with PQ group. Conclusion: These results showed that PQ-induced nephrotoxicity may be caused by oxidative damage in rat kidneys and that M. chamomilla could protect kidneys from PQ-induced toxicity.
  Sami Ghazal , Soleymanian Tayebeh , Khoshraftar Ebrahim and Ranjbar Akram
  Background and Objective: Cisplatin is a widely used chemotherapeutic agent to treat solid tumors. The aim of this study is to evaluate the effects of propofol as a antioxidant on the level of liver enzymes (ALT and AST) in plasma and oxidative damages in liver tissue in rats induced by cisplatin. Methodology: In this study 20 male Wistar rats were at random separated to four groups (n = 4) and then, treated intraperitoneally (IP) for one week. The groups were as follows: Propofol group, control group, cisplatin group, propofol and cisplatin group. Then, propofol was administered (10 mg kg–1 day–1, IP) alone or in mixture with cisplatin (7 mg kg–1 day–1, IP). Also, control group received only normal saline. Oxidative stress parameters, such as: Total Antioxidant Capacity (TAC), catalase (CAT) and total thiol molecules (TTG) in liver tissue and the levels of ALT and AST in serum were measured. Results: Cisplatin hepatotoxicity was manifested by an increase in serum ALT and AST and decrease in TAC in liver tissues. Serum ALT was found to decreased significantly (p<0.008) in the combination group (propofol+cisplatin) in comparison with the cisplatin group. Conclusion: In conclusion, the present results suggest that propofol decrease liver injury induced by cisplatin treatment in liver rats. Further study is needed to clarify the pharmacological significance of its effects on cisplatin poisoning.
 
 
 
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