Yu Zhang1,2, Fang Hu1, Jianghua Wen3, Xiaohong Wei1, Yingjuan Zeng1, Ying Sun1, Shunkui Luo1, Liao Sun4. 1. Department of Endocrinology and Metabolism, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China. 2. Department of Dermatology, Dongguan Maternal and Child Health Hospital, Dongguan, China. 3. Department of Health Examination, Jiangmen Central Hospital, Jiangmen, China. 4. Department of Endocrinology and Metabolism, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China. liaosun520@163.com.
Abstract
BACKGROUND: Ischemia-reperfusion (I/R) injury is the main reason of acute renal failure. However, inflammatory response and cell apoptosis are important mechanisms implicated in I/R injury. Recent studies indicated that nuclear factor kappa B (NF-кB) and tumor necrosis factor α (TNF-α) are both involved in these mechanisms. Sevoflurane reduces NF-кB and TNF-α expression in rats' heart and decreases their renal I/R injury. However, few studies are available regarding the effect of sevoflurane on kidney of diabetic rats. Therefore, the aim of this study was to evaluate sevoflurane effect on NF-кB and TNF-α expression in diabetic rats to decrease renal I/R injury. METHODS: Male Sprague-Dawley rats were divided into five groups: Group A, non-diabetic rats underwent sham operation; Group B, non-diabetic rats with renal I/R injury; Group C, diabetic rats underwent sham operation; Group D, diabetic rats with renal I/R injury; Group E, diabetic rats with renal I/R injury after sevoflurane pretreatment. Rats of Group E were exposed to 2.5% sevoflurane for 30 min. After 24 h, creatinine (Cr), blood urea nitrogen (BUN), renal cell apoptosis, and NF-кB and TNF-α expression in kidney were assessed. RESULTS: Renal cell apoptosis, NF-кB, and TNF-α expression were significantly higher in diabetic rats with renal I/R injury group compared to diabetic rats that underwent sham operation (P < 0.01). These changes were significantly reduced by sevoflurane (P < 0.01). CONCLUSION: Sevoflurane exerted a protective effect against renal injury by lowering the expression of NF-кB and TNF-α in renal I/R diabetic rats.
BACKGROUND:Ischemia-reperfusion (I/R) injury is the main reason of acute renal failure. However, inflammatory response and cell apoptosis are important mechanisms implicated in I/R injury. Recent studies indicated that nuclear factor kappa B (NF-кB) and tumor necrosis factor α (TNF-α) are both involved in these mechanisms. Sevoflurane reduces NF-кB and TNF-α expression in rats' heart and decreases their renal I/R injury. However, few studies are available regarding the effect of sevoflurane on kidney of diabeticrats. Therefore, the aim of this study was to evaluate sevoflurane effect on NF-кB and TNF-α expression in diabeticrats to decrease renal I/R injury. METHODS: Male Sprague-Dawley rats were divided into five groups: Group A, non-diabeticrats underwent sham operation; Group B, non-diabeticrats with renal I/R injury; Group C, diabeticrats underwent sham operation; Group D, diabeticrats with renal I/R injury; Group E, diabeticrats with renal I/R injury after sevoflurane pretreatment. Rats of Group E were exposed to 2.5% sevoflurane for 30 min. After 24 h, creatinine (Cr), blood ureanitrogen (BUN), renal cell apoptosis, and NF-кB and TNF-α expression in kidney were assessed. RESULTS: Renal cell apoptosis, NF-кB, and TNF-α expression were significantly higher in diabeticrats with renal I/R injury group compared to diabeticrats that underwent sham operation (P < 0.01). These changes were significantly reduced by sevoflurane (P < 0.01). CONCLUSION:Sevoflurane exerted a protective effect against renal injury by lowering the expression of NF-кB and TNF-α in renal I/R diabeticrats.
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