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| Circumin attenuates high glucose-induced H9C2 cardiomyocyte injury via NF-κB signaling pathway |
| Hits 848 Download times 555 Received:August 08, 2021 |
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| DOI
10.11656/j.issn.1673-9043.2021.06.21 |
| Key Words
curcumin;cardiomyocytes;inflammation;oxidative stress;NF-κB |
| Author Name | Affiliation | | XIA Juan | Tangshan Nanhu Hospital, Tangshan 063000, China | | ZHANG Shuchun | Tangshan Nanhu Hospital, Tangshan 063000, China | | DAI Ziyang | North China University of Science and Technology, Tangshan 063000, China | | WANG Ya | North China University of Science and Technology, Tangshan 063000, China |
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| Abstract
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| [Objective] To observe the effects of curcumin on inflammation,oxidative and NF-κB signaling pathway to explore its action mechanism of alleviating H9C2 cell injury induced by high glucose.[Methods] Injured model of H9C2 cardiomyocyte was induced by high glucose. The normal control group,model control group and curcumin groups of different concentration (2.5,5,10,20 μmol/L) were set in this experiment. ELISA was used to determine the content of TNF-α,IL-6 and LDH in the cell culture supernatant,and contents of MDA and SOD in H9C2 cardiomyocyte. Western Blot was used to detect the protein expression levels of IKKβ,NF-κB p65 and p-NF-κB p65 in cells.[Results] High glucose treatment on H9C2 cardiomyocytes significantly down-regulated cell viability(P<0.05), the content of TNF-α,IL-6 and LDH in the cell culture supernatant were increased (P<0.05),the MDA content was increased and the SOD content was decreased in H9C2 cardiomyocyte (P<0.05);the protein expression of IKKβ,and p-NF-κB p65 were increased (P<0.05) in the model control group. Pretreatment with circumin (2.5,5,10,20 μmol/L) for 6h significantly maintained cell viability,reduced the content of TNF-α,IL-6 and LDH in the cell culture supernatant (P<0.05),and decreased the MDA content and increased the SOD content in H9C2 cardiomyocyte; down-regulated protein expression levels of IKKβ and p-NF-κB p65 (P<0.05).[Conclusion] Curcumin alleviates high glucose-induced H9C2 cardiomyocyte injury by inhibiting the excessive activation of IKK/NF-κB pathway,and alleviating inflammation and oxidative stress. |
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