Wang Hongyang, Fang Zuochun, Qiu Guoqiang, Zhang Chuang, Tang Min, Zhou Bin
Department of Emergency, The First People's Hospital of Linhai, 317000, Linhai, Zhejiang, China.
Department of Intensive care medicine, Zhejiang Cangnan TCM Hospital, 325800, Cangnan, Zhejiang, China.
Dokl Biochem Biophys. 2021 Sep;500(1):408-414. doi: 10.1134/S1607672921050033. Epub 2021 Oct 25.
Acute kidney injury (AKI), one of the frequently diagnosed and serious sepsis induced complication has high morbidity and mortality. The present study investigated the bioprotective and functional effect of carnosine on AKI induced pathological damage in Male Albino rat model in vivo. AKI in Albino rats was induced by cecal ligation and puncture surgery where as TNF-α and IL-1β levels were detected using ELISA assay. Protein expression was examined by western blotting and pathological damage using hematoxylin and eosin (H&E). Treatment with carnosine suppressed AKI induced urea nitrogen and creatinine in Male Albino rat serum in dose-dependent manner. Development of sepsis mediated renal injury in Albino rats was also effectively prevented on treatment with carnosine. Secretion of AKI-induced IL-1β, IL-18, and TNF-α in renal tissues was alleviated significantly in Albino rats by carnosine treatment. Additionally, in carnosine-treated Albino rats renal tissues AKI induced Bax expression was alleviated while as Bcl-2 was promoted compared to AKI Albino rats. Carnosine treatment improved the survival rate of the Albino rats with AKI. Carnosine inhibits renal tissue damage and increases survival rate in AKI Albino rat model. The mechanism involves alleviation of inflammatory cytokine secretion and promotion of Bcl-2 expression. Thus, carnosine may be used as a therapeutic agent for treatment of AKI.
急性肾损伤（AKI）是脓毒症常见且严重的并发症之一，发病率和死亡率都很高。本研究在雄性白化病大鼠体内模型中，探讨了肌肽对AKI所致病理损伤的生物保护作用及功能影响。通过盲肠结扎和穿刺手术诱导白化病大鼠发生AKI，并用酶联免疫吸附测定（ELISA）法检测肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）水平。采用蛋白质印迹法检测蛋白表达，并用苏木精-伊红（H&E）染色观察病理损伤。肌肽治疗可剂量依赖性地抑制雄性白化病大鼠血清中AKI诱导的尿素氮和肌酐水平。肌肽治疗还能有效预防白化病大鼠脓毒症介导的肾损伤。肌肽治疗可显著减轻白化病大鼠肾组织中AKI诱导的IL-1β、IL-18和TNF-α的分泌。此外，与发生AKI的白化病大鼠相比，经肌肽治疗的白化病大鼠肾组织中，AKI诱导的Bax表达减轻，而Bcl-2表达增加。肌肽治疗提高了发生AKI的白化病大鼠的存活率。肌肽可抑制肾组织损伤并提高AKI白化病大鼠模型的存活率。其机制包括减轻炎性细胞因子分泌及促进Bcl-2表达。因此，肌肽可作为治疗AKI的一种治疗药物。
