Hot Pepper Extract Protects against Hypoglycemia-Induced Brain and Liver Injury in Mice

O. Abdel-Salam, A. Sleem, E. Youness, F. Morsy, Nermeen M. Shaffie, A. Souleman
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引用次数: 3

Abstract

This study aimed to investigate the potential neuroprotective effect of red hot pepper (Capsicum annuum) extract in hypoglycemic injury in mice. Hypoglycemia was induced by intraperitoneal (ip) injection of insulin (3 IU/kg) followed 30 min later by ip administration of the pepper extract at 0.25 and 0.5 g/kg. Mice were euthanized 3 h after insulin injection and their brains were dissected out for biochemical studies including determination of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide, paraoxonase-1 (PON-1), 5-lipoxygenase, and cholinesterase. Histological investigations for the brain and liver, and brain immunohistochemistry (glial fibrillary acidic protein; GFAP) were carried out. Results indicated that hypoglycemia significantly increased MDA and nitric acid levels and decreased GSH content in the brain. There was also significant inhibition of PON-1 and cholinesterase activities, but increased brain 5-lipoxygenase. Spongiform degeneration, vacuolations, and necrotic and apoptotic neurons were seen in the cerebral cortex. Glial cells were markedly decreased both in number and size with decreased GFAP staining. Additionally, necrosis of hepatocytes, and cytoplasmic vacuoles were observed. The biochemical alterations induced by hypoglycemia in the brain tissue were alleviated by the pepper extract resulting in decreased MDA and nitric oxide levels, restoration of GSH content, increased PON-1 and cholinesterase activities, and inhibition of 5-lipoxygenase. The pepper extract reduced the extent of damage to cortical neurons and increased the number, size, and length of astrocytes processes and GFAP expression. In addition, there was marked improvement in pathological changes induced by hypoglycemia in the liver by administering the pepper extract. The study indicates a protective effect for the hot pepper extract against brain and liver damage induced by hypoglycemia likely via inhibition of oxidative stress and 5-lipoxygenase.
辣椒提取物对小鼠低血糖性脑和肝损伤的保护作用
本研究旨在探讨红辣椒提取物对小鼠低血糖损伤的潜在神经保护作用。先腹腔注射胰岛素(3 IU/kg), 30 min后腹腔注射辣椒提取物(0.25和0.5 g/kg)诱导低血糖。注射胰岛素3 h后处死小鼠,解剖小鼠脑进行生化研究,包括测定丙二醛(MDA)、还原型谷胱甘肽(GSH)、一氧化氮、对氧磷酶-1 (PON-1)、5-脂氧合酶和胆碱酯酶。脑、肝组织学检查及脑免疫组化(胶质纤维酸性蛋白;GFAP)。结果表明,低血糖显著提高大鼠脑组织丙二醛和硝酸水平,降低GSH含量。PON-1和胆碱酯酶活性也明显受到抑制,但脑5-脂氧合酶活性升高。大脑皮层可见海绵状变性、空泡形成、神经元坏死和凋亡。胶质细胞数量和大小均明显减少,GFAP染色降低。肝细胞坏死,胞浆空泡增多。辣椒提取物减轻了低血糖引起的脑组织生化改变,降低了MDA和一氧化氮水平,恢复了GSH含量,增加了PON-1和胆碱酯酶活性,抑制了5-脂合酶。辣椒提取物降低了皮质神经元的损伤程度,增加了星形胶质细胞突起的数量、大小和长度以及GFAP的表达。此外,辣椒提取物对肝脏低血糖引起的病理改变也有明显改善。该研究表明,辣椒提取物可能通过抑制氧化应激和5-脂氧合酶,对低血糖引起的脑和肝损伤具有保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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