ArticleImmunity, inflammation and disease2023
Hesperetin attenuates LPS-induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Hesperetin modulates osteoprogenitor cells and macrophages under zoledronic acid and inflammatory stress.Archives of oral biology · 2026Article
- Immunomodulatory and dentinogenic potential of surface-engineered hesperetin-functionalized composite scaffolds for pulp-dentin regeneration.Materials today. Bio · 2026Article
- Syringaldehyde Alleviates Cardiac Hypertrophy Induced by Hyperglycemia in H9c2 Cells Through GLP-1 Receptor Signals.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Evaluating metabolic changes in H9c2 cardiomyoblasts exposed to LPS: Towards understanding sepsis mechanisms.PloS one · 2025Article
- Hesperetin attenuates LPS-induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway.Immunity, inflammation and disease · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
introductionHesperetin (HES), whose main pharmacological effects are anti-inflammatory and cardioprotective properties. In our study, we investigated the role of HES in lipopolysaccharide (LPS)-induced inflammation and apoptosis in H9c2 cells.
methodsCell viability was assessed through MTT assay. Tumor necrosis factor (TNF)-α and interleukin (IL)-β expression were quantified through RT-qPCR assay. Secondly, the apoptosis rate was assessed by Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. Finally, B-cell lymphoma 2 (Bcl-2)- associated X protein (Bax), adenosine monophosphate-activated protein kinase (AMPK), and P53 expression were quantified through western blot assay.
resultsOur results demonstrated that LPS stimulation decreased the cell viability, increased IL-1β and TNF-α expression in H9c2 cells. However, HES treatment significantly increased the cell viability, decreased IL-1β and TNF-α expression in LPS-induced H9c2 cells. In addition, HES significantly increased the phosphorylation level of AMPK. Meanwhile, HES prevented against LPS-mediated the P53 and Bax protein upregulation, and Bcl-2 protein downregulation in H9c2 cells. More interestingly, compound C (an AMPK inhibitor) treatment eliminated the protective effects of HES.
conclusionOur findings revealed that HES attenuated the LPS-mediated inflammation and apoptosis of H9c2 cells by activating the AMPK/P53 signaling pathway, suggesting that HES may be a potential cardioprotective agent.
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