Fu Song, Lv Renhua, Wang Longqiang, Hou Haitao, Liu Haijun, Shao Shize
Department of Spinal, The Wendeng Osteopathic Hospital, Weihai City, Shandong Province 264400, China.
Department of Orthopaedics, Wendeng Central Hospital, Weihai City, Shandong Province 264400, China.
Saudi J Biol Sci. 2018 Feb;25(2):259-266. doi: 10.1016/j.sjbs.2016.10.019. Epub 2016 Nov 4.
Resveratrol, a polyphenol found in various plants, including grapes, plums and peanuts has shown various medIRInal properties, including antioxidant, protection of cardiovascular disease and cancer risk. However, the effects of resveratrol on spinal cord reperfusion injury have not been investigated. Hence, the present study was designed to evaluate the effect of resveratrol on nitric oxide synthase (iNOS)/p38MAPK signaling pathway and to elucidate its regulating effect on the protection of spinal cord injury. Spinal cord ischemia-reperfusion injury (IRI) was performed by the infrarenal abdominal aorta with mini aneurysm clip model. The expressions of iNOS and p38MAPK and the levels of biochemical parameters, including nitrite/nitrate, malondialdehyde (MDA), advanced oxidation products (AOPP), reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were measured in control and experimental groups. IRI-induced rats treated with 10 mg/kg resveratrol protected spinal cord from ischemia injury as supported by improved biological parameters measured in spinal cord tissue homogenates. The resveratrol treatment significantly decreased the levels of plasma nitrite/nitrate, iNOS mRNA and protein expressions and phosphorylation of p38MAPK in IRI-induced rats. Further, IRI-produced free radicals were reduced by resveratrol treatment by increasing enzymatic and non-enzymatic antioxidant levels such as GSH, SOD and CAT. Taken together, administration of resveratrol protects the damage caused by spinal cord ischemia with potential mechanism of suppressing the activation of iNOS/p38MAPK pathway and subsequent reduction of oxidative stress due to IRI.
白藜芦醇是一种存在于多种植物(包括葡萄、李子和花生)中的多酚,已显示出多种药用特性,包括抗氧化、预防心血管疾病和癌症风险。然而,白藜芦醇对脊髓再灌注损伤的影响尚未得到研究。因此,本研究旨在评估白藜芦醇对一氧化氮合酶(iNOS)/p38丝裂原活化蛋白激酶(p38MAPK)信号通路的影响,并阐明其对脊髓损伤保护作用的调节机制。采用肾下腹主动脉夹闭微型动脉瘤模型制作脊髓缺血再灌注损伤(IRI)。检测对照组和实验组中iNOS和p38MAPK的表达以及生化参数水平,包括亚硝酸盐/硝酸盐、丙二醛(MDA)、晚期氧化产物(AOPP)、还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)。用10mg/kg白藜芦醇处理IRI诱导的大鼠,可保护脊髓免受缺血损伤,这在脊髓组织匀浆中检测到的改善的生物学参数得到了支持。白藜芦醇治疗显著降低了IRI诱导大鼠血浆中亚硝酸盐/硝酸盐水平、iNOS mRNA和蛋白表达以及p38MAPK的磷酸化。此外,白藜芦醇治疗通过提高酶促和非酶促抗氧化剂水平(如GSH、SOD和CAT)降低了IRI产生的自由基。综上所述,白藜芦醇的给药可保护脊髓缺血造成的损伤,其潜在机制是抑制iNOS/p38MAPK通路的激活以及随后减少IRI引起的氧化应激。