Protective Mechanism of Banxia Houputang on Lipopolysaccharide-induced Neuroinflammatory Injury
10.13422/j.cnki.syfjx.20220509
- VernacularTitle:半夏厚朴汤对脂多糖诱导神经炎症损伤的保护机制
- Author:
Hui-lin SU
1
;
Ya-ming CHEN
2
;
Hao-dong BAI
2
;
Yu-xing WANG
1
;
Yuan-ning ZENG
1
;
Qiu-hong WANG
1
Author Information
1. Guangdong Engineering Technology Research Center for Standardized Processing of Chinese Herbal Decoction Pieces，School of Traditional Chinese Medicine（TCM），Guangdong Pharmaceutical University，Guangzhou 510006，China
2. Heilongjiang Key Laboratory of TCM Pharmacodynamic Material Bases and Natural Medicines，Key Laboratory of Northern Medicine Foundation and Application，Ministry of Education， Heilongjiang University of Chinese Medicine，Harbin 150040，China
- Publication Type:Journal Article
- Keywords:
Banxia Houputang;
microglia （BV2）;
human neuroblastoma （SH-SY5Y）;
neuroinflammation;
neuroprotection
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(9):1-8
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo study the inhibitory effect of Banxia Houputang （BHT） on lipopolysaccharide （LPS）-induced inflammation of microglia （BV2） cells and the neuroprotective effect on human neuroblastoma （SH-SY5Y） cells. MethodAfter the neuroinflammatory model was constructed by LPS inducing BV2 cells， model group （LPS 100 µg·L-1）， administration groups （LPS+1 g·L-1 BHT， LPS+2 g·L-1 BHT， LPS+5 g·L-1 BHT， LPS+10 g·L-1 BHT）， and blank group were given DEME medium at the same volume. In addition， neuronal apoptosis model was established by co-culture of LPS-induced BV2 cell inflammation medium and SH-SY5Y cells （LPS-DMEM） and was administrated according to the above grouping. Cell viability was detected by Cell Counting Kit-8 （CCK-8） assay. The content of nitric oxide （NO） and that of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） were determined by Griess aasay and enzyme-linked immunosorbent assay （ELISA）， respectively. The mRNA levels of TNF-α， IL-1β， interleukin-4 （IL-4）， nitric oxide synthase （iNOS）， and interleukin-10 （IL-10） were measured by real-time polymerase chain reaction （Real-rime PCR）. Western blot was used to detect the expression levels of signal transducer and activator of transcription 3 （STAT3）， Janus kinase 2 （JAK2） and nuclear factor kappa-B （NF-κB p65）， protein kinase B （Akt）， inhibitor of nuclear factor κB α （IκBα）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2 associated X protein （Bax）. ResultCompared with blank group， LPS increased the NO release， levels of TNF-α， IL-1β， IL-6， and iNOS and protein expression of Akt， NF-κB p65， IκBα， JAK2 and STAT3， decreased the content of IL-4 and IL-10 in BV2 cells， and induced apoptosis of co-cultured SH-SY5Y cells （P<0.01）. Compared with model group， BHT reduced the content of NO， TNF-α， IL-1β， and iNOS （P<0.01） and protein expression of Akt， NF-κB p65， IκBα， JAK2 and STAT3 （P<0.01）， elevated the content of IL-4 and IL-10 （P<0.01）， and inhibited the apoptosis of SH-SY5Y cells induced by LPS-DMEM （P<0.01）. ConclusionThis experiment reveals that BHT inhibited LPS-induced inflammation in BV2 cells by regulating Akt/NF-κB/JAK2/STAT3 signaling pathway and showed neuroprotective effects on SH-SY5Y cells.
