Isochlorogenic acid A alleviates reticulum stress induced by peste des petits rumi-nants virus via PERK signaling pathway
10.16303/j.cnki.1005-4545.2024.07.10
- VernacularTitle:异绿原酸A通过PERK信号通路缓解小反刍兽疫病毒诱导的内质网应激
- Author:
Yun MU
1
;
Tiantian SUN
;
Yongsheng KUANG
;
Shuyi YUAN
;
Yanfen LIU
;
Shaohong CHEN
;
You LIU
;
Fucheng GUO
Author Information
1. 广东海洋大学滨海农业学院,广东湛江 524088
- Keywords:
isochlorogenic acid A(IAA);
peste des petits ruminant virus(PPRV);
reticulum stress(ERS);
PERK signaling pathway
- From:
Chinese Journal of Veterinary Science
2024;44(7):1408-1417
- CountryChina
- Language:Chinese
-
Abstract:
Viral infection can induce endoplasmic reticulum stress(ERS)and unfolded protein re-sponse(UPR)in host cells,resulting in perturbation of endoplasmic reticulum homeostasis.To e-lucidate the action mechanism of isochlorogenic acid A(IAA)in regulating peste des petits rumi-nant virus(PPRV)-induced ERS and UPR,MTT assay,indirect immunofluorescence assay and Western blot were used to evaluate the anti-PPRV activity of IAA,and the effects of IAA on PPRV-induced ERS and PERK signaling pathway were studied by Western blot and quantitative real-time PCR.The results showed that the PPRV replication and virus-induced cytopathic in LDG-2 cells were significantly inhibited,and the survival rate of virus-infected cells was significantly in-creased due to IAA treatment.Compared with the virus control group,the expression levels of GRP78 and p-eIF2α,the ratios of p-PERK/PERK and p-eIF2α/eIF2α in IAA treated PPRV-infec-ted cells were significantly decreased.The expression level of GADD153 significantly decreased at 24,36 h,and significantly increased at 48,60 h.Furthermore,treatment with ERS inhibitor 4-PBA could significantly suppress the expression levels of GRP78,PPRV-N protein and GADD153 in PPRV-infected cells,and the ratios of p-eIF2α/eIF2α and p-PERK/PERK in PPRV-infected cells were also significantly decreased caused by treatment with IAA or 4-PBA and IAA combination.These findings implicated that the PPRV-induced ERS could be alleviated by inhibiting activation of the PERK-eIF2α-GADD1 53 signaling pathway,which led to restriction of PPRV replication in host cells.
