Salvianolic acid B protects against lipopolysaccharide-induced behavioral deficits and neuroinflammatory response: involvement of autophagy and NLRP3 inflammasome.
Salvianolic acid B protects against lipopolysaccharide-induced behavioral deficits and neuroinflammatory response: involvement of autophagy and NLRP3 inflammasome.
复制标题
丹酚酸 B 可防止脂多糖诱导的行为缺陷和神经炎症反应：自噬和 NLRP3 炎性体的参与。
DOI：
10.1186/s12974-017-1013-4
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发表时间：
2017-12-06
影响因子：
9.3
通讯作者：
Xu P
中科院分区：
文献类型：
--
作者：
Jiang P;Guo Y;Dang R;Yang M;Liao D;Li H;Sun Z;Feng Q;Xu P
The NLRP3 inflammasome activation and neuroinflammation are known to be involved in the pathology of depression, whereas autophagy has multiple effects on immunity, which is partly mediated by the regulation of inflammasome and clearance of proinflammatory cytokines. Given the emerging evidence that autophagy dysfunction plays an essential role in depression, it is very likely that autophagy may interact with the inflammatory process in the development and treatment of depression. Salvianolic acid B (SalB), a naturally occurring compound extracted from Salvia miltiorrhiza, contains anti-inflammatory and antidepression properties and has recently been proven to modulate autophagy. In this study, we sought to investigate whether autophagy is involved in the inflammation-induced depression and the antidepressant effects of SalB. The effects of prolonged lipopolysaccharide (LPS) treatment and SalB administration on behavioral changes, neuroinflammation, autophagic markers and NLRP3 activation in rat hippocampus were determined by using behavioral tests, real-time PCR analysis, western blot, and immunostaining. Our data showed that periphery immune challenge by LPS for 2 weeks successfully induced the rats to a depression-like state, accompanied with enhanced expression of pro-inflammatory cytokines and NLRP3 inflammasome activation. Interestingly, autophagic markers, including Beclin-1, and the ratio of LC3II to LC3I were suppressed following prolonged LPS exposure. Meanwhile, co-treatment with SalB showed robust antidepressant effects and ameliorated the LPS-induced neuroinflammation. Additionally, SalB restored the compromised autophagy and overactivated NLRP3 inflammasome in LPS-treated rats. Collectively, these data suggest that autophagy may interact with NLRP3 activation to contribute to the development of depression, whereas SalB can promote autophagy and induce the clearance of NLRP3, thereby resulting in neuroprotective and antidepressant actions.
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DOI：
10.1038/nri.2016.100
发表时间：
2016-11
期刊：
Nature reviews. Immunology
影响因子：
--
作者：
Cadwell K
通讯作者：
Cadwell K
Foxo3a 依赖性 Bim 转录通过促进 Kupffer 细胞中的自噬流来抑制 NLRP3 炎症小体的激活，从而保护小鼠免受高脂肪饮食的影响
影响因子：
--
作者：
Liu Y;Zhang W;Wu X;Gong J
通讯作者：
Gong J
影响因子：
13.3
作者：
Giegerich, Annika Klara;Kuchler, Laura;von Knethen, Andreas
通讯作者：
von Knethen, Andreas
影响因子：
3.4
作者：
Jiang, Pei;Xue, Ying;Zhang, Li-Hong
通讯作者：
Zhang, Li-Hong
影响因子：
7.3
作者：
Keller CW;Lünemann JD
通讯作者：
Lünemann JD