Anti-inflammatory effects of kaempferol-3-O-rhamnoside on HSV-1 encephalitis in vivo and in vitro. (20th November 2021)

• Record Type: Journal Article
• Authors: Zhao, Chaoyang; Wang, Fen; Tang, Bolin; Han, Jun; Li, Xiang; Lian, Guo; Li, Xiaolong; Hao, Shisheng
• Is Part Of: Neuroscience letters. Volume 765(2021)
• Publication Date: 2021-11-20
• Subjects: Herpes simplex virus -- Cytokines -- Apoptosis -- Caspase -- Kaempferol-3-O-rhamnoside; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2021.136172
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: This study showed that K-3-rh had a inhibitory effect on pro-inflammatory cytokines. This experiment found that K-3-rh can reduce the level of NO released by microglia. This study found that K-3-rh had anti-free radical and anti-inflammatory effects. The study showed that K-3-rh could promote virus-induced apoptosis of microglia cells. The study showed that K-3-rh could inhibit the resulting immune damage. Abstract: Background: Herpes simplex virus encephalitis (HSE) is an acute central nervous system infectious disease caused by herpes simplex virus (HSV). Currently, there is no effective treatment for HSE infection, which produces many pro-inflammatory factors. Kaempferol-3-O-rhamnoside (K-3-rh) is a plant flavonoid. This study was investigated the anti-inflammatory effect of K-3-rh on encephalitis induced by HSV-1. Methods: HSV-1 was co-cultured with VERO cells. Cells were divided into four groups, including the control group, virus group, K-3-rh group, Astragalus polysaccharide (APS) group and dexamethasone group. Flow cytometry were utilized to determine cell apoptosis, respectively. Proteins and mRNAs were estimated by western blot and qRT-PCR, respectively. Results: After viral infection, the cytokines were significantly increased. After K-3-rh intervention, the expression of tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), and nitric oxide (NO) in microglia were reduced contrast with those in the virus group, and the expression of interleukin-10 (IL-10) did not change. After viral infection, the apoptotic rate increased significantly, and K-3-rh could inhibit viral-induced apoptosis in the microglial cell line. The induction of microglia apoptosis was achieved by cytochrome c and caspase-9-mediated mitochondrial pathway. Also, the pathological changes of brain tissue in mice of each drug intervention group were alleviated. Conclusions: In conclusion, K-3-rh had the potential to reduce HSV-1-induced brain injury by reducing the secretion of microglial pro-inflammatory factors, inducing apoptosis of microglia cells, and through cytochrome C and caspase-3 pathway.