发酵薄荷给药通过下调 MAPK 信号通路对沙土鼠和 SH-SY5Y 细胞短暂全脑缺血发挥神经保护作用。
Fermented Mentha arvensis administration provides neuroprotection against transient global cerebral ischemia in gerbils and SH-SY5Y cells via downregulation of the MAPK signaling pathway.
机构信息
Department of Veterinary Medicine and Biosafety Research Institute, Jeonbuk National University, 79 Gobong-to, Iksan, Jeollabuk-do, Republic of Korea, 54596.
Department of Pharmacology and Toxicology, Faculty of Veterinary, Animal and Biomedical Sciences, Sylhet Agricultural University, Sylhet, 3100, Bangladesh.
出版信息
BMC Complement Med Ther. 2022 Jun 25;22(1):172. doi: 10.1186/s12906-022-03653-7.
BACKGROUND
Globally, ischemic stroke is a major health threat to humans that causes lifelong disability and death. Mentha arvensis (MA) has been used in traditional medicine to alleviate oxidative stress and inflammation-related disorders. In the present study, the neuroprotective properties of fermented MA (FMA) extract were investigated in the gerbil and SH-SY5Y cells. model of transient global cerebral ischemia.
METHODS
Bilateral common carotid artery occlusion-induced transient global cerebral ischemia in gerbil and hydrogen peroxide (HO)-mediated neurotoxic effects in human neuroblastoma cells (SH-SY5Y) were investigated. FMA (400 mg/kg) was orally administered for 7 days before induction of ischemic stroke. To evaluate the neuroprotective activity of FMA, we implemented various assays such as cell viability assay (MTT), lactate dehydrogenase (LDH) assay, histopathology, immunohistochemistry (IHC), histofluorescence, and western blot.
RESULTS
FMA pretreatment effectively decreased transient ischemia (TI) induced neuronal cell death as well as activation of microglia and astrocytes in the hippocampal region. The protective effects of FMA extract against HO-induced cytotoxicity of SH-SY5Y cells were observed by MTT and LDH assay. However, FMA pretreatment significantly increased the expression of the antioxidant marker proteins such as superoxide dismutase-1 (SOD-1) and superoxide dismutase-2 (SOD-2) in the hippocampus and SH-SY5Y cells. Furthermore, the activation of mitogen-activated protein kinase (MAPK) further activated a cascade of outcomes such as neuroinflammation and apoptosis. FMA pretreatment notably decreased TI and HO induced activation of MAPK (c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinase (ERK), and p38) proteins in hippocampus and SH-SY5Y cells respectively. Besides, pretreatment with FMA markedly reduced HO mediated Bax/Bcl2 expression in SH-SY5Y cells.
CONCLUSION
Thus, these results demonstrated that neuroprotective activities of FMA might contribute to regulating the MAPK signaling pathway.
背景
在全球范围内，缺血性中风是对人类健康的主要威胁，会导致终身残疾和死亡。薄荷（MA）已在传统医学中用于缓解氧化应激和炎症相关疾病。在本研究中，研究了发酵薄荷（FMA）提取物在沙鼠和 SH-SY5Y 细胞中的神经保护特性。模型中的短暂性全脑缺血。
方法
在沙鼠中进行双侧颈总动脉闭塞诱导的短暂性全脑缺血和过氧化氢（HO）介导的人神经母细胞瘤细胞（SH-SY5Y）神经毒性作用，并进行研究。在诱导缺血性中风前 7 天口服给予 FMA（400mg/kg）。为了评估 FMA 的神经保护活性，我们实施了各种测定，如细胞活力测定（MTT）、乳酸脱氢酶（LDH）测定、组织病理学、免疫组织化学（IHC）、组织荧光和 Western blot。
结果
FMA 预处理可有效减少短暂性缺血（TI）诱导的神经元细胞死亡以及海马区小胶质细胞和星形胶质细胞的激活。MTT 和 LDH 测定观察到 FMA 提取物对 HO 诱导的 SH-SY5Y 细胞细胞毒性的保护作用。然而，FMA 预处理显著增加了海马和 SH-SY5Y 细胞中抗氧化标记蛋白的表达，如超氧化物歧化酶-1（SOD-1）和超氧化物歧化酶-2（SOD-2）。此外，丝裂原激活蛋白激酶（MAPK）的激活进一步激活了神经炎症和细胞凋亡等级联反应。FMA 预处理显著降低了 TI 和 HO 诱导的海马和 SH-SY5Y 细胞中 MAPK（c-Jun N-末端激酶（JNK）、细胞外信号调节蛋白激酶（ERK）和 p38）蛋白的激活。此外，FMA 预处理显著降低了 HO 介导的 SH-SY5Y 细胞中 Bax/Bcl2 表达。
结论
因此，这些结果表明 FMA 的神经保护活性可能有助于调节 MAPK 信号通路。
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