Investigating the effect of ethanolic extract of Commiphora myrrha (Nees) Engl. gum-resin against hepatorenal injury in diabetic rats

没药醇提物树脂对糖尿病大鼠肝肾损伤的保护作用研究

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作者:Mohammadmehdi Hassanzadeh-Taheri, Mojtaba Salimi, Khadijeh Vazifeshenas-Darmiyan, Mahtab Mohammadifard, Mehran Hosseini

Conclusions

These findings demonstrated that EEM treatment at doses up to 500 mg/kg could not effectively slow down the pathological process of hepatorenal damage in diabetic rats.

Methods

Diabetes was induced by an intraperitoneal (i.p.) injection of streptozotocin (55 mg/kg) in adult male Wistar rats (n = 40); whereas, normal control rats (NC, n = 8) were treated with vehicle solution (citrate buffer, i.p.). Diabetic animals were gavaged with 500 mg/kg of metformin (MET500) and different doses of EEM (100, 300, and 500 mg/kg) once daily for 28 days. Diabetic model (DM) and NC groups were treated with normal saline. Various parameters like fasting blood glucose (FBG), plasma insulin, aspartate transaminase (AST), alanine transaminase (ALT), creatinine (Cr), urea, 24-h urine total protein (UTP), urine volume, and hepatorenal histopathology were assessed at the end of the study.

Purpose

Management of hepatorenal complications in diabetic patients is still a challenge for clinicians. The study aimed to investigate the impacts of ethanolic extract of Commiphora myrrha (Nees) Engl.oleo-gum-resin (EEM) against hepatorenal injury in diabetic rats.

Results

Compared to the NC group, diabetic rats showed marked elevations in FBG, AST, ALT, urea, Cr, UTP, urine volume, and a significant reduction in insulin. Diabetic animals also exhibited severe histopathological alterations in liver and kidney tissues. The EEM treatment could not influence the biochemical and pathological alterations. Treatment with EEM at the dose of 300 mg/kg could slightly ameliorate some pathological alterations (fatty changes and tubular congestion) in hepatic and renal tissues. Conclusions: These findings demonstrated that EEM treatment at doses up to 500 mg/kg could not effectively slow down the pathological process of hepatorenal damage in diabetic rats.

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