Aloe-emodin inhibits African swine fever virus replication by promoting apoptosis via regulating NF-κB signaling pathway

• Published in: Virology journal Vol. 20; no. 1; p. 158
• Main Authors: Luo, Yizhuo, Yang, Yunlong, Wang, Wenru, Gao, Qi, Gong, Ting, Feng, Yongzhi, Wu, Dongdong, Zheng, Xiaoyu, Zhang, Guihong, Wang, Heng
• Format: Journal Article
• Language: English
• Published: England BioMed Central 19.07.2023; BMC
• Subjects: active ingredients; African Swine Fever; African swine fever virus; African Swine Fever Virus - genetics; Aloe - metabolism; Aloe-emodin; Alveoli; Animals; Antiviral activity; Antiviral Agents - pharmacology; Antiviral drugs; antiviral properties; Apoptosis; Asfarviridae; Bcl-2 protein; Emodin; Emodin - pharmacology; Epidemics; fever; Flow cytometry; fluorescent antibody technique; Hemorrhage; Hemorrhagic fever; Hogs; Immunofluorescence; Infections; Inflammation; Influenza; Infrared imaging systems; Interleukin 8; Macrophages; mechanism of action; MyD88 protein; NF-kappa B - metabolism; NF-κB protein; NF-κB signaling pathway; Nitric oxide; Proteins; quantitative polymerase chain reaction; Replication; Signal Transduction; Swine; therapeutics; Transcriptomics; Virus Replication; Western blotting; United Kingdom > UK; United States > US; China; African swine fever virus; Aloe-emodin; NF-κB signaling pathway; Apoptosis
• ISSN: 1743-422X; 1743-422X
• DOI: 10.1186/s12985-023-02126-8

African swine fever (ASF) is an acute infectious haemorrhagic fever of pigs caused by African swine fever virus (ASFV). Aloe-emodin (Ae) is an active ingredient of Chinese herbs with antiviral, anticancer, and anti-inflammatory effects. We investigated the antiviral activity and mechanism of action of Ae against ASFV using Real-time quantitative PCR (qPCR), western blotting, and indirect immunofluorescence assays. Ae significantly inhibited ASFV replication. Furthermore, transcriptomic analysis revealed that ASFV infection activated the NF-κB signaling pathway in the early stage and the apoptosis pathway in the late stage. Ae significantly downregulated the expression levels of MyD88, phosphor-NF-κB p65, and pIκB proteins as well as the mRNA levels of IL-1β and IL-8 in porcine alveolar macrophages (PAMs) infected with ASFV, thereby inhibiting the activation of the NF-κB signaling pathway induced by ASFV. Flow cytometry and western blot analysis revealed that Ae significantly increased the percentage of ASFV-induced apoptotic cells. Additionally, Ae promoted apoptosis by upregulating the expression levels of cleaved-caspase3 and Bax proteins and downregulating the expression levels of Bcl-2 proteins. This suggests that Ae promotes apoptosis by inhibiting the NF-κB pathway, resulting in inhibition of ASFV replication. These findings have further improved therapeutic reserves for the prevention and treatment of ASF.