Neuroprotective Activity of Premna latifolia on Streptozotocin Induced Diabetic Neuropathy in Rats

Neelakanth M. Jeedi, S. K. Nimbal, Santosh B Patil
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Abstract

The leaves of plant Premna latifolia Lam are traditionally used for treating diabetes and related complications. Presently ethanolic extract of leaves of plant P. latifolia explored for the neuroprotective potential in rat model of streptozotocin induced diabetic neuropathy. The intra-peritoneal route administered streptozotocin 60 mg/kg body weight to induce experimental diabetes, then treatment were not given for two weeks to develop diabetic complications. After two weeks of induction, animals were treated with extract 100 and 200 mg/kg per day for the duration of five weeks. The neuroprotective effect was assessed using Eddy’s hot plate and tail immersion method. Also, measuring blood sugar and cytokines cause inflammations like interleukins, tumor necrosis factor and a neurotrophin in the sciatic nerve. Thiobarbituric acid reactive substances reduced glutathione and activity levels of catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase measured in the sciatic tissue. Extract normalizes blood glucose in diabetic neuropathy rats brought on by streptozotocin. The diabetic neuropathy rats show significant reductions in the period when the tail retracts and the paws are licked or jumped. In these rats pro-inflammatory cytokines level in sciatic nerve was significantly high. In addition, the oxidative stress bio-markers level altered significantly in sciatic nerve tissue. Diabetic neuropathy-developing rats treated with extract for five weeks reduce the levels of nerve growth factor, oxidative stress indicators, and pro-inflammatory cytokines rise in the sciatic nerve tissue. Ethanolic extract of P. latifolia possesses neuroprotective action in streptozotocin-induced diabetic neuropathy.
厚朴对链脲佐菌素诱导的糖尿病大鼠神经病变的神经保护作用
植物 Premna latifolia Lam 的叶子传统上用于治疗糖尿病及相关并发症。目前,研究人员正在探索花叶薄荷叶乙醇提取物在链脲佐菌素诱导的糖尿病神经病变大鼠模型中的神经保护潜力。通过腹腔注射链脲佐菌素 60 毫克/千克体重来诱导实验性糖尿病,然后在两周内不给予治疗,以防止糖尿病并发症的发生。诱导两周后,动物每天分别接受 100 毫克和 200 毫克/千克提取物的治疗,持续五周。采用艾迪热板法和尾部浸泡法评估神经保护作用。此外,还测量了血糖和引起坐骨神经炎症的细胞因子,如白细胞介素、肿瘤坏死因子和一种神经营养素。测量坐骨神经组织中硫代巴比妥酸活性物质还原谷胱甘肽以及过氧化氢酶、超氧化物歧化酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶的活性水平。提取物能使链脲佐菌素引起的糖尿病神经病变大鼠的血糖恢复正常。糖尿病神经病变大鼠在尾巴缩回、爪子被舔或跳动时,血糖会明显降低。这些大鼠坐骨神经中的促炎细胞因子水平明显偏高。此外,坐骨神经组织中的氧化应激生物标志物水平也发生了显著变化。用提取物治疗糖尿病神经病变大鼠五周后,坐骨神经组织中的神经生长因子、氧化应激指标和促炎细胞因子水平均有所降低。白花蛇舌草乙醇提取物对链脲佐菌素诱导的糖尿病神经病变具有神经保护作用。
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