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首页> 外文期刊>Journal of Pharmacy and Pharmacology >Study of nuclear factor-2 erythroid related factor-2 activator, berberine, in paclitaxel induced peripheral neuropathy pain model in rats
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Study of nuclear factor-2 erythroid related factor-2 activator, berberine, in paclitaxel induced peripheral neuropathy pain model in rats

机译:核因子2红细胞相关因子-2活化剂,小檗碱,紫杉醇诱导大鼠外周神经病变疼痛模型的研究

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Objectives The role of nuclear factor-2 erythroid related factor-2 (Nrf2) activator, berberine (BBR), has been established in rat model of streptozotocin induced diabetic neuropathy. Around 30-40% of cancer patients, on paclitaxel (PTX) chemotherapy develop peripheral neuropathy. The present study was contemplated with the aim of establishing the neuropathy preventive role of BBR, in paclitaxel induced peripheral neuropathy model in rats. Methods A total of 30 Wistar rats were divided into five groups as follows: Group I: dimethyl sulfoxide; Group II: PTX+ 0.9% NaCl; Group III: Amitriptyline (ATL) + PTX; Group IV: BBR (10 mg/kg) + PTX and Group V: BBR (20 mg/kg) + PTX. Animals were assessed for tail flick latency, tail cold allodynia latency, histopathological scores, oxidative stress parameters, and mRNA expression of the Nrf2 gene in the sciatic nerve. Key findings Berberine significantly increased the tail flick and tail cold allodynia latencies and significantly decreased the histopathological score. BBR reduced oxidative stress by significantly decreasing the lipid peroxidation, increasing the superoxide dismutase and reduced glutathione levels in the sciatic nerve. BBR also increased the mRNA expression of Nrf2 gene in rat sciatic nerve. Conclusions All of these results showed the neuropathy preventing role of BBR in PTX induced neuropathy pain model in rats.
机译:目标核因子-2红细胞相关因子-2(NRF2)活化剂,Berberine(BBR)的作用已经在链脲佐菌素诱导的糖尿病神经病变的大鼠模型中建立。在紫杉醇(PTX)化疗的癌症患者约有30-40%的癌症患者中发生外周神经病变。本研究旨在旨在建立BBR的神经病预防作用,在大鼠中紫杉醇诱导的外周神经病理模型。方法将总数30只Wistar大鼠分为五组,如下:I基团:二甲基亚砜; II组:PTX + 0.9%NaCl;第三组:amitiptyline(ATL)+ PTX;第IV组:BBR(10mg / kg)+ PTX和G组:BBR(20mg / kg)+ PTX。评估动物尾巴延迟,尾部冷异步疼痛,组织病理学评分,氧化应激参数和坐骨神经中NRF2基因的mRNA表达。主要发现者小檗碱显着增加了尾巴轻质和尾状异常患者潜伏期,显着降低了组织病理学分数。 BBR通过显着降低脂质过氧化,增加超氧化物歧化酶并降低坐骨神经中的谷胱甘肽水平来降低氧化应激。 BBR还增加了大鼠坐骨神经中NRF2基因的mRNA表达。结论所有这些结果表明BBR在大鼠PTX诱导神经病理疼痛模型中的神经病预防。

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