مقالههای Aghdas Dehghani
توجه: محتویات این صفحه به صورت خودکار پردازش شده و مقالههای نویسندگانی با تشابه اسمی، همگی در بخش یکسان نمایش داده میشوند.
نویسنده(ها): Fatemeh Motamedi، Mehdi Nematbakhsh *، Ramesh Monajemi، Zahra Pezeshki، Ardeshir Talebi، Behzad Zolfaghari، Azam Mansoori، Shadan Saberi، Aghdas Dehghani، Farzaneh Ashrafi،
اطلاعات انتشار: Journal of nephropathology، سوم،شماره۴، Oct ۲۰۱۴، سال ۰
تعداد صفحات: ۶
Background: Chemotherapy with cisplatin (CP) is accompanied with nephrotoxicity.Objectives: In the current study, pomegranate flower extract (PFE) has been evaluated as anantioxidant agent against CP–induced–renal toxicity.Materials and Methods: Thirty two male Wistar rats were divided into five groups (6–8 in eachgroup). The animals in groups 1 to 3 received PFE (25 mg\kg), PFE (50 mg\kg), and placebo(saline), respectively for 9 days, and onset of the day 3, they also received CP (2.5 mg\kg\day). Groups 4 and 5 were treated with PFE (25 and 50 mg\kg\day) for 9 days. Finally,the animals were sacrificed at day 9 after collecting blood samples. Kidneys were removed,weighted, and underwent histopathological investigation.Results: The mean serum level of creatinine in group 3 (treated with CP and placebo) increasedsignificantly (p0.05), but the value decreased significantly (p0.05) in group 1. Kidneyweight in group 1 was lower than KW in groups 2 and 3, however it was significant whencompared with group 2 (p0.05). The serum nitrite level in group 2 was non–significantlylower than that in other groups, and no significant changes were observed in serum levelsof malondialdehyde (MDA). Tissue level of nitrite was significantly decreased in the positivecontrol and high dose of PFE plus CP–treated groups (p0.05). Among CP–treated groups,low dose of PFE significantly improved kidney nitrite level (p0.05). The results fromhistopathological staining indicated less tissue damage in group 1 when compared withgroup 3.Conclusions: It seems that low dose of PFE plays a protective role against CP–induced renaltoxicity in rats.
۲Role of Mas receptor in renal blood flow response to angiotensin–(1–7) in ovariectomized estradiol treated rats
اطلاعات انتشار: Research in Pharmaceutical Sciences، يازدهم،شماره۱(پياپي ۳۴)، ۲۰۱۶، سال ۰
تعداد صفحات: ۸
The angiotensin 1–7 (Ang 1–7), is abundantly produced in kidneys and antagonizes the function of angiotensin II through Mas receptor (MasR) or other unknown mechanisms. In the current study, the role of MasR and steroid hormone estrogen on renal blood flow response to Ang 1–7 administration was investigated in ovariectomized (OV) female rats. OV female Wistar–rats received estradiol (500 µg\kg\week) or vehicle for two weeks. In the day of the experiment, the animals were anesthetized, cannulated, and the responses including mean arterial pressure, renal blood flow (RBF), and renal vascular resistance at the constant level of renal perfusion pressure to graded infusion of Ang 1–7 at 0, 100 and 300 ng\kg\min were determined in OV and OV estradiol–treated (OVE) rats, treated with vehicle or MasR antagonist; A779. RBF response to Ang 1–7 infusion increased dose–dependently in vehicle (Pdose0.001) and A779–treated (Pdose0.01) animals. However, when MasR was blocked, the RBF response to Ang 1–7 significantly increased in OV animals compared with OVE rats (P0.05). When estradiol was limited by ovariectomy, A779 increased RBF response to Ang 1–7 administration, while this response was attenuated in OVE animals.
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