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首页> 外文期刊>The Internet Journal of Pharmacology >Effect of antioxidants such as β-carotene, vitamin C and vitamin E on oxidative stress, thermal hyperalgesia and cold allodynia in streptozotocin induced diabetic rats
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Effect of antioxidants such as β-carotene, vitamin C and vitamin E on oxidative stress, thermal hyperalgesia and cold allodynia in streptozotocin induced diabetic rats

机译：β-胡萝卜素，维生素C和维生素E等抗氧化剂对链脲佐菌素诱导的糖尿病大鼠氧化应激，热痛觉过敏和冷异常性疼痛的影响

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A study was undertaken to evaluate the effect of antioxidants such as β-carotene, vitamin C and vitamin E on oxidative stress, thermal hyperalgesia and cold allodynia in streptozotocin induced diabetic rats. The hyperalgesia and allodynia was assessed by estimating tail withdrawal latency in warm and cold water immersion method. Furthermore, serum TBARS and plasma GSH levels were estimated to assess the oxidative stress. Treatment with β-carotene (10 mg/kg/day i.p.), vitamin C (10 mg/kg/day i.p.) and vitamin E (40 mg/kg/day i.p.) showed significant ameliorative effects on thermal hyperalgesia and cold allodynia in streptozotocin induced diabetic rats. Moreover, treatment with β-carotene markedly prevented thermal hyperalgesia and cold allodynia in streptozotocin induced diabetic rats. Address of Research Work Department of Pharmacology, I.S.F. College of Pharmacy, Moga, Punjab-142 001, India Introduction Diabetes is a global health problem and its prevalence is set to increase to 366 million worldwide by the year 2025 1 . Persistent hyperglycemia in diabetic patients, despite, appropriate therapeutic measures leads to several complications including retinopathy, nephropathy and neuropathy. Diabetic neuropathy is the most common complication affecting more than 50% of the diabetic patients. The symptoms of diabetic neuropathy includes pain, parathesia and aberrant, hyperalgesia, allodynia, loss of sensory perception, muscle weakness reduction in motor nerve conduction velocity. 234 Hyperalgesia is exaggerated response to painful stimuli which is due to reduction in pain threshold and allodynia is nocifensive response to normally innocuous stimuli. 5 Etiology of diabetic neuropathy is complex and multifactorial. Diabetic neuropathy involves complex molecular mechanisms such as auto oxidative glycosylation, formation of glycation products, activation of protein kinase-C, polyol pathway, mitogen activated protein kinases (MAPK), poly (ADP-ribose) polymerase (PARP) and Nicotinamide Adenine Di-nucleotide Phosphate (NADPH) oxidase and induction of oxidative stress. 6789 Oxidative stress is a common link between all these pathways and is a major contributor to the development of neuropathy and hyperalgesia in diabetes. 1011 Oxidative stress occurs in a cellular system due to the imbalance between the generation of reactive oxygen species (ROS) & decrease in amount of antioxidant system to neutralize ROS such as superoxide (O2ˉ), hydrogen peroxide (H2O2), hydroxyl radical (OHˉ), peroxinitrite (ONOOˉ), reactive aldehydes & lipid peroxides. 1213 Once formed, reactive oxygen species deplete antioxidant defenses (glutathione (GSH) peroxidase, superoxide dismutase and catalase) and render the cells and tissues vulnerable to oxidative damage. 14 Lipids, proteins and DNA are the cellular targets for the oxidative stress and leads to alteration in cellular structure and functions. Oxidative stress activates downstream pathways such as mitogen-activated protein kinases (MAPK), poly (ADP-ribose) polymerase (PARP) and NADPH oxidase. 15 Recent evidences suggest that reactive oxygen species act as second messenger in the regulation of intracellular signaling pathways and ultimately, gene expression. 16 Increased oxidative stress causes vascular impairment leading to endoneurial hypoxia resulting in impaired neural function, reduced nerve conduction velocity and loss of neurotrophic support. 17 Thus, oxidative stress is the one of the potential targets for diabetic neuropathy.β-carotene, vitamin C and vitamin E are natural antioxidants normally found in diet that scavenges reactive oxygen species. In the present study, we have investigated the effect of β-carotene, vitamin C and vitamin E on hyperalgesia and allodynia in streptozotocin induced diabetic rats by assessing nociception, intracellular antioxidants and oxidative stress. Materials and Methods MaterialsStreptozotocin and β-carotene were purchased from Sigma Chemicals (Missouri, USA), Vitami
机译：进行了一项研究，以评估抗氧化剂（如β-胡萝卜素，维生素C和维生素E）对链脲佐菌素诱发的糖尿病大鼠的氧化应激，热痛觉过敏和冷异常性疼痛的作用。通过估计在温水和冷水浸泡方法中的尾巴撤回潜伏期来评估痛觉过敏和异常性疼痛。此外，估计血清TBARS和血浆GSH水平以评估氧化应激。用β-胡萝卜素（10 mg / kg /天ip），维生素C（10 mg / kg / day ip）和维生素E（40 mg / kg / day ip）治疗对链脲佐菌素对热痛觉过敏和冷异常性疼痛有明显的改善作用诱导的糖尿病大鼠。此外，用β-胡萝卜素治疗可显着预防链脲佐菌素诱发的糖尿病大鼠的热痛觉过敏和冷异常性疼痛。 I.S.F.药理学研究部门的地址莫加药学院，印度旁遮普邦142 001导言糖尿病是一个全球性的健康问题，到2025年，糖尿病的患病率将在全球范围内增加至3.66亿1。尽管采取适当的治疗措施，糖尿病患者中的持续性高血糖症也会导致多种并发症，包括视网膜病变，肾病和神经病。糖尿病性神经病是影响50％以上糖尿病患者的最常见并发症。糖尿病性神经病的症状包括疼痛，感觉异常和异常，痛觉过敏，异常性疼痛，感觉知觉丧失，运动神经传导速度的肌肉无力减少。 [234]痛觉过敏是对疼痛刺激的过度反应，这是由于疼痛阈值降低所致，而异常性疼痛是对通常无害刺激的伤害性反应。 5糖尿病神经病的病因是复杂和多因素的。糖尿病性神经病涉及复杂的分子机制，例如自身氧化糖基化，糖基化产物形成，蛋白激酶C活化，多元醇途径，促分裂原活化蛋白激酶（MAPK），聚（ADP-核糖）聚合酶（PARP）和烟酰胺腺嘌呤二-核苷酸磷酸（NADPH）氧化酶和氧化应激的诱导。 6789氧化应激是所有这些途径之间的共同纽带，并且是糖尿病神经病变和痛觉过敏发展的主要因素。 1011由于活性氧（ROS）的产生与抗氧化剂体系的减少以中和ROS（如过氧化物（O2 system），过氧化氢（H2O2），羟基自由基（OHˉ））之间的不平衡，在细胞系统中发生了氧化应激，过氧亚硝酸盐（ONOOˉ），活性醛和脂质过氧化物。 1213一旦形成，活性氧就会耗尽抗氧化剂的防御能力（​​谷胱甘肽（GSH）过氧化物酶，超氧化物歧化酶和过氧化氢酶），并使细胞和组织容易受到氧化损伤。 14脂质，蛋白质和DNA是氧化应激的细胞靶标，并导致细胞结构和功能的改变。氧化应激激活下游途径，例如丝裂原激活的蛋白激酶（MAPK），聚（ADP-核糖）聚合酶（PARP）和NADPH氧化酶。 15最近的证据表明，活性氧在细胞内信号通路和基因表达的调控中充当第二信使。 16氧化应激增加导致血管损伤，导致神经内膜缺氧，导致神经功能受损，神经传导速度降低和神经营养支持丧失。 17因此，氧化应激是糖尿病性神经病的潜在靶标之一。β-胡萝卜素，维生素C和维生素E是通常在饮食中发现的天然抗氧化剂，可清除活性氧。在本研究中，我们通过评估伤害感受，细胞内抗氧化剂和氧化应激，研究了β-胡萝卜素，维生素C和维生素E对链脲佐菌素诱导的糖尿病大鼠的痛觉过敏和异常性疼痛的作用。材料和方法材料链脲佐菌素和β-胡萝卜素购自Vitami的Sigma Chemicals（美国密苏里州）

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