Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway
Abstract Introduction Hesperetin (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. Methods Cell viability was assessed through MT...
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| Format: | Article |
| Language: | English |
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Wiley
2023-08-01
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| Series: | Immunity, Inflammation and Disease |
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| Online Access: | https://doi.org/10.1002/iid3.973 |
| _version_ | 1827779274631806976 |
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| author | Zan Xie Chunxia Yang Tingting Xu |
| author_facet | Zan Xie Chunxia Yang Tingting Xu |
| author_sort | Zan Xie |
| collection | DOAJ |
| description | Abstract Introduction Hesperetin (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. Methods Cell 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. Results Our 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. Conclusion Our 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. |
| first_indexed | 2024-03-11T14:46:49Z |
| format | Article |
| id | doaj.art-f24f58bae6cd423a995c7deab11f2a53 |
| institution | Directory Open Access Journal |
| issn | 2050-4527 |
| language | English |
| last_indexed | 2024-03-11T14:46:49Z |
| publishDate | 2023-08-01 |
| publisher | Wiley |
| record_format | Article |
| series | Immunity, Inflammation and Disease |
| spelling | doaj.art-f24f58bae6cd423a995c7deab11f2a532023-10-30T10:50:33ZengWileyImmunity, Inflammation and Disease2050-45272023-08-01118n/an/a10.1002/iid3.973Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathwayZan Xie0Chunxia Yang1Tingting Xu2Department of Cardiology the Affiliated Yantai Yuhuangding Hospital of Qingdao University Yantai Shandong ChinaDepartment of Cardiology the Affiliated Yantai Yuhuangding Hospital of Qingdao University Yantai Shandong ChinaDepartment of Cardiology the Affiliated Yantai Yuhuangding Hospital of Qingdao University Yantai Shandong ChinaAbstract Introduction Hesperetin (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. Methods Cell 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. Results Our 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. Conclusion Our 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.https://doi.org/10.1002/iid3.973AMPKapoptosishesperetininflammationlipopolysaccharideP53 |
| spellingShingle | Zan Xie Chunxia Yang Tingting Xu Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway Immunity, Inflammation and Disease AMPK apoptosis hesperetin inflammation lipopolysaccharide P53 |
| title | Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway |
| title_full | Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway |
| title_fullStr | Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway |
| title_full_unstemmed | Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway |
| title_short | Hesperetin attenuates LPS‐induced the inflammatory response and apoptosis of H9c2 by activating the AMPK/P53 signaling pathway |
| title_sort | hesperetin attenuates lps induced the inflammatory response and apoptosis of h9c2 by activating the ampk p53 signaling pathway |
| topic | AMPK apoptosis hesperetin inflammation lipopolysaccharide P53 |
| url | https://doi.org/10.1002/iid3.973 |
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