Pal Pabitra Bikash, Pal Sankhadeep, Manna Prasenjit, Sil Parames C
Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata 700054, West Bengal, India.
Pathophysiology. 2012 Apr;19(2):101-14. doi: 10.1016/j.pathophys.2012.02.001. Epub 2012 Mar 15.
The present study has been carried out to investigate the role of the aqueous extract of the fruits of Pithecellobium dulce (AEPD) against carbon tetrachloride (CCl(4)) induced renal oxidative injury in mice. HPLC analysis shows that AEPD contains phenolics, flavonoids and saponins as the major active components. Creatinine and blood urea nitrogen (BUN) levels were assayed to determine renal protective action of AEPD in CCl(4)-induced renal pathophysiology. Its antioxidant activity was determined by measuring radical scavenging activity, antioxidant enzymes activities, GSH content, protein carbonylation and lipid peroxidation. In addition, FACS analysis, DNA fragmentation and histological studies were carried out to determine its effect in CCl(4) induced renal oxidative injury and cell death. CCl(4) exposure increased the intracellular reactive oxygen species production, decreased intracellular antioxidant defence, reduced mitochondrial membrane potential, attenuated the intracellular ATP content and caused renal cell death mainly via the necrotic pathway as revealed by DNA fragmentation analysis. Treatment with AEPD both prior and post to the toxin exposure protected the organ from CCl(4) induced oxidative insult. Histological studies also support our results. Combining, results suggest that the protective role of AEPD against CCl(4) induced renal oxidative impairments is probably due to the antioxidative properties present in its active constituents.
本研究旨在探讨猴耳环果实水提取物(AEPD)对四氯化碳(CCl₄)诱导的小鼠肾氧化损伤的作用。高效液相色谱分析表明,AEPD含有酚类、黄酮类和皂苷类作为主要活性成分。检测肌酐和血尿素氮(BUN)水平以确定AEPD在CCl₄诱导的肾脏病理生理学中的肾脏保护作用。通过测量自由基清除活性、抗氧化酶活性、谷胱甘肽含量、蛋白质羰基化和脂质过氧化来确定其抗氧化活性。此外,进行流式细胞术分析、DNA片段化和组织学研究以确定其在CCl₄诱导的肾氧化损伤和细胞死亡中的作用。如DNA片段化分析所示,CCl₄暴露增加了细胞内活性氧的产生,降低了细胞内抗氧化防御能力,降低了线粒体膜电位,减弱了细胞内ATP含量,并主要通过坏死途径导致肾细胞死亡。在毒素暴露前后用AEPD处理可保护器官免受CCl₄诱导的氧化损伤。组织学研究也支持我们的结果。综合来看,结果表明AEPD对CCl₄诱导的肾氧化损伤的保护作用可能归因于其活性成分中存在的抗氧化特性。