2013Chinese Journal of Geriatric CareRequires access

Protective effects of Shenkang injection against gentamicin-induced kidney injury in rat

Yan-Yan Deng

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Abstract

Objective To investigate effects and its mechanism of Shenkang injection against gentamicin-induced kidney injury. Methods Thirty female Sprague-Dawley rats were randomly divided into sham operation group,model group and treatment group, with 10 rats in each group. Rats in model group and treatment group were given intraperitoneal injection of gentamicin 100mg / ( kg· d) to establish model of acute kidney injury. Rats in treatment group were given intraperitoneal injection of Shenkang injection 2g / ( kg·d) and rats in model group were given intraperitoneal injection of 0. 9% sodium chloride injection 6. 67ml/( kg·d) ,and rats in sham operation group were given twice intraperitoneal injection of 0. 9% sodium chloride injection with 2. 25ml / ( kg · d) , 6. 67ml / ( kg·d) . All rats administered for 7 consecutive days. Blood levels of urea nitrogen and creatinine,pathological changes of kidney were observed,activity of superoxide dismutase and glutathione peroxidase and content of malondialdehyde in renal tissue were detected on the 8th day. Results Swelling and focal necroses of renal tubular epithelial cell,destruction of renal tubule wall were observed in model group,and renal pathological changes were milder in treatment group compared to those in model group. Compared to sham operation group,blood levels of urea nitrogen and creatinine,content of malondialdehyde in renal tissue were higher and activity of superoxide dismutase and glutathione peroxidase in renal tissue were lower in model group( P 0. 05,respectively) . And in treatment group,blood levels of urea nitrogen and creatinine,content of malondialdehyde in renal tissue were lower and activity of superoxide dismutase and glutathione peroxidase in renal tissue were higher compared to model group( P 0. 05,respectively) . Conclusion Shenkang injection could alleviate gentamicin-induced kidney injury in rat via abatement of oxidative stress in renal tissues.

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Objective To investigate effects and its mechanism of Shenkang injection against gentamicin-induced kidney injury. Methods Thirty female Sprague-Dawley rats were randomly divided into sham operation group,model group and treatment group, with 10 rats in each group. Rats in model group and treatment group were given intraperitoneal injection of gentamicin 100mg / ( kg· d) to establish model of acute kidney injury. Rats in treatment group were given intraperitoneal injection of Shenkang injection 2g / ( kg·d) and rats in model group were given intraperitoneal injection of 0. 9% sodium chloride injection 6. 67ml/( kg·d) ,and rats in sham operation group were given twice intraperitoneal injection of 0. 9% sodium chloride injection with 2. 25ml / ( kg · d) , 6. 67ml / ( kg·d) . All rats administered for 7 consecutive days. Blood levels of urea nitrogen and creatinine,pathological changes of kidney were observed,activity of superoxide dismutase and glutathione peroxidase and content of malondialdehyde in renal tissue were detected on the 8th day. Results Swelling and focal necroses of renal tubular epithelial cell,destruction of renal tubule wall were observed in model group,and renal pathological changes were milder in treatment group compared to those in model group. Compared to sham operation group,blood levels of urea nitrogen and creatinine,content of malondialdehyde in renal tissue were higher and activity of superoxide dismutase and glutathione peroxidase in renal tissue were lower in model group( P 0. 05,respectively) . And in treatment group,blood levels of urea nitrogen and creatinine,content of malondialdehyde in renal tissue were lower and activity of superoxide dismutase and glutathione peroxidase in renal tissue were higher compared to model group( P 0. 05,respectively) . Conclusion Shenkang injection could alleviate gentamicin-induced kidney injury in rat via abatement of oxidative stress in renal tissues.

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Available abstract

Objective To investigate effects and its mechanism of Shenkang injection against gentamicin-induced kidney injury. Methods Thirty female Sprague-Dawley rats were randomly divided into sham operation group,model group and treatment group, with 10 rats in each group. Rats in model group and treatment group were given intraperitoneal injection of gentamicin 100mg / ( kg· d) to establish model of acute kidney injury. Rats in treatment group were given intraperitoneal injection of Shenkang injection 2g / ( kg·d) and rats in model group were given intraperitoneal injection of 0. 9% sodium chloride injection 6. 67ml/( kg·d) ,and rats in sham operation group were given twice intraperitoneal injection of 0. 9% sodium chloride injection with 2. 25ml / ( kg · d) , 6. 67ml / ( kg·d) . All rats administered for 7 consecutive days. Blood levels of urea nitrogen and creatinine,pathological changes of kidney were observed,activity of superoxide dismutase and glutathione peroxidase and content of malondialdehyde in renal tissue were detected on the 8th day. Results Swelling and focal necroses of renal tubular epithelial cell,destruction of renal tubule wall were observed in model group,and renal pathological changes were milder in treatment group compared to those in model group. Compared to sham operation group,blood levels of urea nitrogen and creatinine,content of malondialdehyde in renal tissue were higher and activity of superoxide dismutase and glutathione peroxidase in renal tissue were lower in model group( P 0. 05,respectively) . And in treatment group,blood levels of urea nitrogen and creatinine,content of malondialdehyde in renal tissue were lower and activity of superoxide dismutase and glutathione peroxidase in renal tissue were higher compared to model group( P 0. 05,respectively) . Conclusion Shenkang injection could alleviate gentamicin-induced kidney injury in rat via abatement of oxidative stress in renal tissues.

Key concepts: Malondialdehyde, Intraperitoneal injection, Blood urea nitrogen, Medicine, Creatinine, Kidney, Glutathione peroxidase, Superoxide dismutase

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