Immunity, inflammation and disease · 2023
Fisetin regulates the biological effects of rat nucleus pulposus mesenchymal stem cells under oxidative stress by sirtuin-1 pathway.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zhou Qing, Zhu Chao, Xuan Anwu, Zhang Junyou, Zhu Zhenbiao, Tang Liang, Ruan Dike
Аннотация
BACKGROUND: Excessive oxidative stress has been accepted as one of the critical factors for intervertebral disc degeneration (IDD), which is associated with low back pain (LBP). Fisetin (Fis) is a bioactive flavonoid that possesses strong bioactive activity. In present study, we aimed to illuminate the role of Fis on nucleus pulposus mesenchymal stem cells (NPMSCs).
METHODS: NPMSCs were isolated and cultured from rat NP tissues and identified by flow cytometry and multilinear differentiation. The cytotoxicity of Fis, EX-527, and hydrogen peroxide (H2 O2 ) on NPMSCs was validated using Cell Counting Kit-8 tests. Cell apoptosis was tested by flow cytometry and TUNEL assay. Inflammatory mediators were assessed by Elisa tests, RT-PCR. Extracellular matrix (ECM) metabolism was measured by Western blot analysis and RT-qPCR. The expression of the SIRT1 was evaluated by Western blot analysis.
RESULTS: NPMSCs were successfully isolated and cultured from rat NP tissues, and it has been identified by flow cytometry and multilinear differentiation. The results showed that Fis attenuated H2 O2 -induced apoptosis, inflammation, and ECM degradation of NPMSCs. Moreover, the above protective effects of Fis can be inhibited by EX-527, a unique SIRT1 inhibitor, indicating that SIRT1 may involve in the mechanism of Fis in protecting NPMSCs from oxidative stress.
CONCLUSIONS: As a natural compound with little cytotoxicity on NPMSCs, Fis alleviate H2 O2 -induced apoptosis, inflammation, and ECM degradation by suppressing oxidative stress, this finding may add the theoretical basis for research on new treatment of IDD based on NPMSCs.
METHODS: NPMSCs were isolated and cultured from rat NP tissues and identified by flow cytometry and multilinear differentiation. The cytotoxicity of Fis, EX-527, and hydrogen peroxide (H2 O2 ) on NPMSCs was validated using Cell Counting Kit-8 tests. Cell apoptosis was tested by flow cytometry and TUNEL assay. Inflammatory mediators were assessed by Elisa tests, RT-PCR. Extracellular matrix (ECM) metabolism was measured by Western blot analysis and RT-qPCR. The expression of the SIRT1 was evaluated by Western blot analysis.
RESULTS: NPMSCs were successfully isolated and cultured from rat NP tissues, and it has been identified by flow cytometry and multilinear differentiation. The results showed that Fis attenuated H2 O2 -induced apoptosis, inflammation, and ECM degradation of NPMSCs. Moreover, the above protective effects of Fis can be inhibited by EX-527, a unique SIRT1 inhibitor, indicating that SIRT1 may involve in the mechanism of Fis in protecting NPMSCs from oxidative stress.
CONCLUSIONS: As a natural compound with little cytotoxicity on NPMSCs, Fis alleviate H2 O2 -induced apoptosis, inflammation, and ECM degradation by suppressing oxidative stress, this finding may add the theoretical basis for research on new treatment of IDD based on NPMSCs.