Mechanism of Buyang-Huanwu Decoction regulating NLRP3 inflammasome mediated inflammation after spinal cord injury
10.3760/cma.j.cn115398-20200108-00050
- VernacularTitle:补阳还五汤调控脊髓损伤后NLRP3炎症体介导炎症反应的机制
- Author:
Jie DING
1
;
Tianrui XU
;
Xiao FAN
Author Information
1. 中国人民解放军陆军第73集团军医院中医康复理疗科，厦门 361003
- From:
International Journal of Traditional Chinese Medicine
2020;42(6):552-556
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the mechanism of Buyang-Huanwu Decoction on inflammation mediated by NOD-like receptors (NLRP3) inflammasome. Methods:A total of 48 rats were divided into sham operation group, model group and Buyang-Huanwu Decoction group, 16 in each group according to the random number table method. The model group and the Buyang-Huanwu Decoction group used spinal cord blowers to hit the spinal cord to establish a spinal cord injury model. The Buyang-Huanwu Decoction group was gavaged with Buyang-Huanwu Decoction 12.6 g/(kg?d), and the sham operation group and the model group were gavaged with equal volume of sterile saline once a day for 3 days. Nissl staining was used to observe the neuronal morphology of spinal cord tissues in each group. Immunohistochemical staining was used to detect the expression of NLRP3 in spinal cord tissues. ELISA was used to detect the levels of serum IL-1β and IL-18. Western blot was used to detect the expression of cleaved systeinyl aspartate-specific protease (cleaved-Caspase1). Results:Compared to the model group, the average optical density of NLRP3 positive expression (0.54 ± 0.04 vs. 0.78 ± 0.06) in Buyang-Huanwu decoction group significantly decreased ( P<0.05); the content of IL-1β (43.66 ± 1.21 pg/ml vs. 67.64 ± 2.43 pg/ml) and IL-18 (49.43 ± 3.88 pg/ml vs. 65.87 ± 2.53 pg/ml) in serum of the Buyang-Huanwu decoction group significantly decreased ( P<0.05); the expression of cleaved caspase 1 protein (0.63 ± 0.02 vs. 0.79 ± 0.07) in Buyang-Huanwu decoction group significantly decreased ( P<0.05). Conclusions:The Buyang-Huanwu Decoction can reduce the inflammatory response by inhibiting the expression of NLRP3 inflammasome after spinal cord injury, by reducing the activation of Caspase1.
