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Resveratrol exerts antiproliferative effects on high-glucose-cultured vascular smooth muscle cells via inhibition of STAT3 and upregulation of mitochondrial gene GRIM-19 which is responsible for STAT3 activation
Background and aim The current study aimed to investigate the antiproliferative effect of Resv on the growth of VSMCs and to determine the association between Resv and STAT3 and the mitochondrial biogenesis signaling pathway under high-glucose conditions. Materials and methods Male Wistar rats weigh...
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Published in: | International journal of diabetes in developing countries 2022-04, Vol.42 (2), p.348-355 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background and aim
The current study aimed to investigate the antiproliferative effect of Resv on the growth of VSMCs and to determine the association between Resv and STAT3 and the mitochondrial biogenesis signaling pathway under high-glucose conditions.
Materials and methods
Male Wistar rats weighing between 180 and 200 g were killed by cervical vertebra dislocation. Primary VSMCs were obtained by outgrowth methods. Cells from different treatment groups were then collected, and changes in cell proliferation and signaling pathway activity were analyzed by PCR and Western blotting. And the MTT assay was used to investigate the effect of Resv on VSMC proliferation.
Results
Resv inhibited proliferation of VSMCs under high-glucose conditions. Resv suppressed the transcriptional activity of STAT3, but the mitochondrial gene GRIM-19, which is responsible for STAT3 activation, was simultaneously upregulated. The mitochondrial biogenesis signaling pathway components NRF1, NRF2, TFB1m, and TFB2m were also upregulated. In addition, the mitochondrial genes NDUFA1, NDUFA2, and NDUFA3 were involved in the function of Resv.
Conclusion
The results of the study suggest that Resv has an antiproliferative effect in high-glucose-cultured VSMCs partly through inhibiting STAT3 function and upregulating mitochondrial biogenesis. |
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ISSN: | 0973-3930 1998-3832 |
DOI: | 10.1007/s13410-021-00963-3 |