Zhang Rui, Liu Cui, Liu Xuejun, Guo Yunliang
Department of ICU, The Affiliated Hospital of Qingdao University Qingdao, China.
Department of Cardiovascular Medicine, The Affiliated Hospital of Qingdao University Qingdao, China.
Am J Transl Res. 2016 Sep 15;8(9):3963-3969. eCollection 2016.
Cerebral ischemia is the major causes the neuronal damages throughout the world. Present investigation evaluates the neuroprotective effect of (SS) in cerebral ischemic rat. All the rats were separated in to four group such as control group, ischemia/reperfusion (I/R) group and (100 and 200 mg/kg, p.o.) treated group which receives extract for 15 days prior to I/R. At the end of protocol all the rats were sacrificed and brain was isolated for the biochemical estimation. Further, oxidative stress was estimated by measuring the level of malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD) and glutathione peroxidase (GPX) in the brain tissue. Moreover other parameters like cytokine (IL-10 and TNF-α), nuclear factor kappa B p65 (NF-κB), caspase 3, brain ATP level and DNA damage by comet assay was estimated in the brain tissues of cerebral ischemic rats. Result of the study suggested that treatment with significantly (P<0.01) decreases the MDA and NO level and increases in the activity of SOD and GPX in the brain tissues of cerebral ischemic rats compared to I/R rats. Moreover, treatment with SS significantly increases the expressions of IL-10 and brain ATP and decreases the expressions of TNF-α, caspase 3 and NF-κB in the brain tissues of cerebral ischemic rats compared to I/R rats. Comet assay also postulates that SS treated rats brain shows less DNA damage than ischemic rats. Present study concludes the neuroprorective effect of in cerebral ischemic rats by its antioxidant, anti apoptotic and anti-inflammatory activity.
脑缺血是全球范围内导致神经元损伤的主要原因。目前的研究评估了(SS)对脑缺血大鼠的神经保护作用。所有大鼠被分为四组,即对照组、缺血/再灌注(I/R)组以及(100和200mg/kg,口服)治疗组,治疗组在I/R前15天接受提取物治疗。实验结束时,处死所有大鼠并分离大脑进行生化评估。此外,通过测量脑组织中丙二醛(MDA)、一氧化氮(NO)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPX)的水平来评估氧化应激。此外,还评估了脑缺血大鼠脑组织中的其他参数,如细胞因子(IL-10和TNF-α)、核因子κB p65(NF-κB)、半胱天冬酶3、脑ATP水平以及彗星试验检测的DNA损伤。研究结果表明,与I/R大鼠相比,(SS)治疗显著(P<0.01)降低了脑缺血大鼠脑组织中的MDA和NO水平,并提高了SOD和GPX的活性。此外,与I/R大鼠相比,SS治疗显著增加了脑缺血大鼠脑组织中IL-10和脑ATP的表达,并降低了TNF-α、半胱天冬酶3和NF-κB的表达。彗星试验还表明,SS治疗的大鼠脑DNA损伤比缺血大鼠少。本研究得出结论,(SS)通过其抗氧化、抗凋亡和抗炎活性对脑缺血大鼠具有神经保护作用。