Periplaneta americana extract ameliorates lipopolysaccharide‑induced liver injury by improving mitochondrial dysfunction via the AMPK/PGC‑1α signaling pathway
- Wei Shi
- Li An
- Jun Zhang
- Jie Li
Affiliations: Department of Geriatrics, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu 210009, P.R. China
- Published online on: August 8, 2021 https://doi.org/10.3892/etm.2021.10572
Copyright: © Shi
et al. This is an open access article distributed under the
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Periplaneta americana (PA) extract acts clinically as a therapeutic treatment in various diseases; it enhances liver function in mouse models and mitigates the pathological condition of liver fibrosis. The present study aimed to investigate the role and potential mechanisms underlying the action of the PA extract, xinmailong (XML), in lipopolysaccharide (LPS)‑induced liver injury. Following the treatment of AML12 cells with LPS, the content of cytochrome c in the cytoplasm and mitochondria, and the level of ATP synthesis were detected using corresponding kits. The relative mRNA expression levels of nuclear respiratory factor 1 and transcription factor A, mitochondrial were investigated using reverse transcription‑quantitative (RT‑q)PCR analysis. The MTT assay was performed to detect the viability of AML12 cells following treatment with XML, in the absence or presence of LPS. Western blot analysis was performed to determine the expression levels of proteins in the AMP‑activated protein kinase (AMPK)/proliferator‑activated receptor γ coactivator‑1α (PGC‑1α) pathway. Following treatment with compound C, an inhibitor of AMPK, the expression levels of inflammatory cytokines were determined using ELISA and RT‑qPCR analysis. The levels of oxidative stress‑related markers were detected using corresponding kits following treatment with compound C. In addition, TUNEL staining was performed to detect the apoptosis of AML12 cells, and western blot analysis was performed to investigate the expression levels of apoptosis‑related proteins. Mitochondrial dysfunction was induced by LPS in AML12 cells. LPS stimulation significantly downregulated the expression of proteins in the AMPK/PGC‑1α pathway, which was reversed following treatment with XML. In addition, inflammation, oxidative stress and mitochondrial dysfunction induced by LPS were alleviated by XML in AML12 cells. However, the addition of compound C and XML to LPS‑induced AML12 cells resulted in the aggravation of cell injury. Collectively, the results of the present study indicated that XML suppressed mitochondrial dysfunction induced by LPS by activating AMPK/PGC‑1α signaling. Thus, the results of the present study may contribute to further understanding of the underlying mechanism via which XML alleviates liver injury.