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Showing 3 results for Hassanshahi

Jalal Hassanshahi, Maryam Maleki, Mehdi Nematbakhsh,
Volume 21, Issue 4 (December 2017)

Unilateral ureteral obstruction (UUO) is a clinical scenario that leads to obstructive nephropathy. UUO alters the expression of many mediators in the ipsilateral kidney. Renin-angiotensin system (RAS) is involved in UUO. Angiotensin II (Ang II) and angiotensin 1-7 (Ang 1-7) as the main arms of RAS influence kidney function which may alter by UUO. Ang II via Ang II receptor subtypes I (AT1R) reduces renal blood flow and glomerular filtration rate and induces oxidative stress, apoptosis as well as inflammation in renal tissue and contributes to renal fibrosis in UUO model. Also, Ang 1-7 receptor (MasR) and Ang II receptor subtype II (AT2R) may have a protective effect against UUO-induced renal injury. In addition, there is crosstalk among RAS with the main vasodilator factors (prostaglandins E2 and I2, bradykinin, atrial natriuretic factor, nitric oxide and adenosine) and the main vasoconstrictor factors (endothelin and vasopressin) in the ipsilateral kidney with UUO. In this review, the roles of the RAS on renal function and its interactions with the other factors in the kidney with UUO were discussed.

Alireza Samimiat, Mohammad Sedigh Khosravi, Jalal Hassanshahi, Mehdi Nematbakhsh,
Volume 22, Issue 2 (June 2018)

Introduction: Renal ischemia-reperfusion (RIR) may disturb renin-angiotensin system components. In this study, the effects of Mas receptor (A779) and AT2 receptor (PD123319) antagonists were examined in RIR rats. Methods: Total 60 male and female Wistar rats were assigned into 10 groups (n=6 in each group), including sham-operated group, RIR groups treated with the vehicle, A779, PD123319, or A779+PD123319. The rats were subjected to 30 minutes renal ischemia followed by 75 minutes reperfusion and the vehicle/antagonists were started to infuse 15 minutes after beginning of reperfusion for 60 min. Mean arterial pressure (MAP) and renal perfusion pressure responses to antagonists were assessed. Measurements for kidney function parameters also were performed. All the measurements were made at the end of 60 min vehicle/antagonist infusion. Results: MAP has altered significantly during RIR times (P=0.004), but no significant difference was observed between two genders. The RIR itself in injured rats (compared to sham operated rats) decreased urine flow (UF), creatinine clearance (Ccr), filtrate load of sodium (FNa) and sodium excretion rate (ENa) significantly in both genders (P<0.05). The antagonists infusion caused significant decrease in Ccr and FNa in male and female rats subjected to RIR when compared with vehicle (P<0.05), but the UF decreased significantly (P<0.05) only in PD123319 treated groups; however, there was no significant difference in ENa between the RIR groups in both genders. Conclusion: Our findings showed the importance role of Mas receptor and AT2 receptor on renal function after kidney ischemia/reperfusion in RIR rat model.

Zahra Taghipour, Elham Kaviani, Ayat Kaeidi, Ali Shamsizadeh, Jalal Hassanshahi, Iman Fatemi,
Volume 23, Issue 1 (March 2019)

Introduction: Atorvastatin (Ator) is a lipid lowering drug with potent antioxidant and anti-inflammatory properties. The present investigation was designed to study the effect of Ator on D-galactose (GAL)-induced hepatorenal toxicity in mice. Methods: In this study, 40 mice were divided into 4 groups: normal, GAL (500 mg/kg), Ator 0.1 (0.1mg/kg)+GAL and Ator 1 (1mg/kg)+GAL. Ator and GAL were administered orally for 6 weeks simultaneously. Then on day 43, blood samples were collected to determine blood urea nitrogen (BUN), serum creatinine (sCr), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. The kidneys and livers samples were used for histological examination. Results: Our results indicated that administration of GAL significantly increases sCr, BUN, ALT and AST. Co-administration of Ator 0.1 and 1mg/kg with GAL for 6 weeks (especially 1mg/kg) attenuated these changes. Histological changes in kidney such as infiltration of leukocyte, necrosis and oedema were observed in GAL group. Moreover, pyknosis, infiltration of inflammatory cell and fat deposit were observed in the livers of GAL-treated mice. Co-administration of Ator 0.1 and 1mg/kg with GAL for 6 weeks (especially 1mg/kg) could mitigate the histological lesions in kidneys and livers of GAL-administered animals. Conclusion: The results of this study suggested that Ator may have beneficial effects on hepatorenal toxicity induced by GAL.

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