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“针刺百会穴(GV 20)、水沟穴(GV 26)、合谷穴(LI 4)、风府穴(GV 16)和哑门穴(GV 15)可降低创伤性脑损伤大鼠模型中脑小胶质细胞的激活。”

"Acupuncture stimulation of Yamen (GV 15), Fengfu (GV 16), Baihui (GV 20), Shuigou (GV 26) and Hegu (LI 4) reduces brain microglia activation in a traumatic brain injury rat model".

机构信息

College of Chinese Medicine, Jinan University, Guangzhou 510632, China.

出版信息

J Tradit Chin Med. 2020 Apr;40(2):267-274.

Abstract

OBJECTIVE

To evaluate the effect of acupuncture on neuroinflammation in traumatic brain injury (TBI) rats by stimulating Yamen (GV 15), Fengfu (GV 16), Baihui (GV 20), Shuigou (GV 26) and Hegu (LI 4) acupoints and to investigate the mechanism underpinning this effect.

METHODS

A TBI model was induced in Sprague- Dawley rats using Feeney's freefall impact method. Acupuncture to stimulate the Yamen (GV 15), Fengfu (GV 16), Baihui (GV 20), Shuigou (GV 26) and Hegu (LI 4) acupoints was performed on the TBI rats. After 3 consecutive days of acupuncture treatment, we investigated signal molecules, receptors and microglia related to neuroinflammation in brain tissue of the TBI rats and analyzed the possible mechanism underlying the effect of acupuncture on neuroinflammation.

RESULTS

After the acupuncture treatment, ionized calcium binding adaptor molecule 1(Iba1), a protein specific to microglia, was investigated. In the cortical layer of damaged brain tissue in TBI rats, the Iba1-positive area was 3.3% ± 0.9% in the rats that received acupuncture compared with 5.2% ± 1.4% in the TBI rats that did not receive acupuncture, and the microglia were smaller with more slender protrusions in the acupuncture-treated rats. This result indicates that acupuncture can significantly reduce microglia activation in TBI rats. A possible mechanism for this effect is that acupuncture reduces the expression of autotaxin and lysophosphatidic acid. Together, these constitute the autotaxin-lysophosphatidic acid axis, which induces microglial activation in the brains of TBI rats. Acupuncture treatment may downregulate the expression of Lysophosphatidic acid (LPA) receptor (LPAR) 1 and LPAR2 on the microglial cytomembrane, which affects the microglia activation process.

CONCLUSION

Acupuncture stimulating the Yamen (GV 15), Fengfu (GV 16), Baihui (GV 20), Shuigou (GV 26) and Hegu (LI 4) acupoints can effectively inhibit the development of neuroinflammation after TBI. One possible mechanism for this effect is that acupuncture downregulates LPA synthesis and affects the LPA-LPAR pathway by inhibiting LPAR1 and LPAR2, thereby inhibiting microglial activation and reducing neuroinflammation.

摘要

目的

通过刺激百会穴(GV 20)、水沟穴(GV 26)、合谷穴(LI 4)等穴位,评价针刺对创伤性脑损伤(TBI)大鼠神经炎症的影响,并探讨其作用机制。

方法

采用 Feeney 自由落体撞击法建立 TBI 大鼠模型。对 TBI 大鼠进行针刺刺激百会穴(GV 20)、水沟穴(GV 26)、合谷穴(LI 4)等穴位的治疗。连续针刺治疗 3 天后,检测 TBI 大鼠脑组织中与神经炎症相关的信号分子、受体和小胶质细胞,并分析针刺治疗对神经炎症影响的可能机制。

结果

针刺治疗后,用离子钙结合衔接分子 1(Iba1)检测小胶质细胞特异性蛋白。在 TBI 大鼠损伤脑组织皮质层中,针刺组 Iba1 阳性面积为 3.3%±0.9%,而未针刺组为 5.2%±1.4%,针刺组小胶质细胞体积较小,突起较细长。这表明针刺能显著减少 TBI 大鼠小胶质细胞的激活。这种作用的可能机制是针刺降低了自分泌酶和溶血磷脂酸的表达。自分泌酶和溶血磷脂酸构成了自分泌酶-溶血磷脂酸轴,诱导 TBI 大鼠脑内小胶质细胞的激活。针刺治疗可能下调小胶质细胞膜上的溶血磷脂酸(LPA)受体(LPAR)1 和 LPAR2 的表达,从而影响小胶质细胞的激活过程。

结论

针刺刺激百会穴(GV 20)、水沟穴(GV 26)、合谷穴(LI 4)等穴位能有效抑制 TBI 后神经炎症的发展。其作用机制之一可能是通过抑制 LPAR1 和 LPAR2 来下调 LPA 的合成,影响 LPA-LPAR 通路,从而抑制小胶质细胞的激活,减轻神经炎症。

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