Pananx notoginseng saponins attenuate CCL2-induced cognitive deficits in rats via anti-inflammation and anti-apoptosis effects that involve suppressing over-activation of NMDA receptors.
Pananx notoginseng saponins attenuate CCL2-induced cognitive deficits in rats via anti-inflammation and anti-apoptosis effects that involve suppressing over-activation of NMDA receptors.
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三七皂苷通过抗炎和抗凋亡作用（包括抑制 NMDA 受体过度激活）减轻 CCL2 诱导的大鼠认知缺陷。
DOI：
10.1016/j.biopha.2020.110139
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发表时间：
2020-04
影响因子：
7.5
通讯作者：
Zhou Yan
中科院分区：
文献类型：
--
作者：
Zhou Yi-Jun;Chen Jian-Min;Sapkota Kiran;Long Jiang-Yi;Liao Yuan-Jun;Jiang Jun-Jun;Liang Bing-Yu;Wei Jin-Bin;Zhou Yan
HIV 相关神经认知障碍 (HAND) 的特点是大脑突触损伤和神经元丢失，最终导致认知能力和记忆力逐渐下降。趋化因子 CC 基序配体 2 (CCL2) 在脑脊液 (CSF) 中升高，并被认为与 HAND 有关。我们的研究团队之前的研究表明，CCL2 增强 N-甲基-D-天冬氨酸受体 (NMDAR) 介导的兴奋性突触后电流 (EPSC) 并导致神经细胞损伤。然而，目前可用于治疗 CCL2 引起的神经损伤的药物很少。三七皂苷 (PNS) 是从三七中分离出来的，对人体有多种益处，包括神经保护作用。然而，PNS 对 CCL2 诱导的神经毒性的保护作用仍不清楚。在这项研究中，我们发现三七总皂苷改善了CCL2诱导的学习和记忆障碍，并抑制CCL2诱导的细胞死亡。这些作用可能是通过减轻谷氨酸代谢功能障碍来抑制 NMDA 受体的过度激活所致。此外，三七总皂苷调节的 CCL2 诱导的细胞内氧化应激可减轻细胞炎症。此外，PNS 预处理通过降低 Bax/BCL-2 比率和 caspase-3、8、9 表达来明显抑制细胞凋亡途径。总之，本研究表明 PNS 对 CCL2 诱导的神经毒性提供了显着的神经保护作用，并且可能是 CCL2 诱导的 HAND 或其他神经退行性疾病的新型治疗剂。
HIV-associated neurocognitive disorders (HAND) are characterized by synaptic damage and neuronal loss in the brain, ultimately leading to progressive decline of cognitive abilities and memory. Chemokine CC motif ligand 2 (CCL2) is elevated in cerebrospinal fluid (CSF), and has been believed to contribute to HAND. Previous studies by our research team have shown that CCL2 enhances N-Methyl-D-aspartate receptor (NMDAR)-mediated excitatory postsynaptic currents (EPSCs) and causes nerve cell damage. However, there are few drugs currently available to treat nerve damage that is caused by CCL2.Panax notoginsengsaponins (PNS) are isolated fromPanax notoginsengand benefit the human body in various ways, including the neuroprotective effect. However, the protective effect of PNS on CCL2-induced neurotoxicity remains unknown. In this study, we found that PNS improved CCL2-induced learning and memory impairment, and inhibited CCL2-induced cell death. These effects may be due to inhibiting over-activation of NMDA receptors by alleviating the dysfunction of glutamate metabolism. Furthermore, PNS-modulated CCL2-inducd intracellular oxidative stress was found to attenuate cell inflammation. Additionally, PNS pretreatment evidently inhibited apoptotic pathways by reducing the Bax/BCL-2 ratio and caspase-3, 8, 9 expressions. In conclusion, this study demonstrates that PNS provides substantial neuroprotection against CCL2-induced neurotoxicity, and may be a novel therapeutic agent in CCL2-induced HAND or other neurodegenerative diseases.
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影响因子：
5.4
作者：
Shiyun Wang;Minghong Li;Ying Guo;Chen Li;Lanou Wu;Xin-Fu Zhou;Yaohui Luo;D. An;Shude Li;Haiyun Luo;Lijin Pu
通讯作者：
Shiyun Wang;Minghong Li;Ying Guo;Chen Li;Lanou Wu;Xin-Fu Zhou;Yaohui Luo;D. An;Shude Li;Haiyun Luo;Lijin Pu
影响因子：
5.3
作者：
Sandy Stayte;Kathryn J. Laloli;Peggy Rentsch;A. Lowth;Kong M. Li;R. Pickford;B. Vissel
通讯作者：
Sandy Stayte;Kathryn J. Laloli;Peggy Rentsch;A. Lowth;Kong M. Li;R. Pickford;B. Vissel
影响因子：
5.3
作者：
Rubio FJ;Ampuero E;Sandoval R;Toledo J;Pancetti F;Wyneken U
通讯作者：
Wyneken U
影响因子：
6.1
作者：
Chompre G;Cruz E;Maldonado L;Rivera-Amill V;Porter JT;Noel RJ Jr
通讯作者：
Noel RJ Jr
DOI：
10.4049/jimmunol.1302647
发表时间：
2015-04-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Carvallo L;Lopez L;Che FY;Lim J;Eugenin EA;Williams DW;Nieves E;Calderon TM;Madrid-Aliste C;Fiser A;Weiss L;Angeletti RH;Berman JW
通讯作者：
Berman JW