Tetrahydroxy stilbene glucoside alleviates palmitic acid-induced inflammation and apoptosis in cardiomyocytes by regulating miR-129-3p/Smad3 signaling

Abstract

Objective Tetrahydroxy stilbene glucoside (TSG) has been reported to exert a cytoprotective effect against various toxicants. However, the function and mechanism of TSG in palmitic acid (PA)-induced inflammation and apoptosis in cardiomyocytes are still unknown. The present study was designed to investigate the post-transcriptional mechanism in TSG-treated cardiomyocytes’ inflammation and apoptosis induced by PA. Methods The mRNA and protein levels were assayed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. Cell proliferation was analyzed by CCK-8 assay. Annexin V-fluorescein isothiocyanate/polyimide (annexin V-FITC/PI) staining was used to evaluate apoptosis using flow cytometry. Results TSG restricted the detrimental effects, including the activated inflammatory response and apoptosis, of PA in cardiomyocytes, as well as the up-regulation of miR-129-3p and down-regulation of p-Smad3 expression. In addition, bioinformatics and experimental analysis suggested that Smad3 was a direct target of miR-129-3p, which could inhibit or enhance the expression of p-Smad by transfection with miR-129-3p mimics or inhibitors, respectively. Furthermore, our results demonstrated that overexpression of Smad3 reversed the inhibition of inflammation and apoptosis by overexpression of miR-129-3p in PA-stimulated cardiomyocytes. Conclusion TSG targeted to miR-129-3p/Smad3 signaling inhibited PA-induced inflammation and apoptosis in cardiomyocytes.

MicroRNA-129-5p alleviates spinal cord injury in mice via suppressing the apoptosis and inflammatory response through HMGB1/TLR4/NF-κB pathway

“…For example, Li et al reported that miR-129-5p suppressed the spinal cord ischemia-reperfusion (IR) injury-induced inflammation in mice by inhibiting HMGB1 and the TLR3-cytokine pathway [35]. Notably, Zou et al showed that miR-129-5p overexpression inhibited the inflammation and apoptosis in palmitic acid (PA)-induced cardiomyocyte injury model [45]. As we known, apoptosis is another key process that influences the development of neuronal tissue damage following SCI [13].…”

Circular RNA SIPA1L1 promotes osteogenesis via regulating the miR-617/Smad3 axis in dental pulp stem cells

“…In a similar way, Smad3 was discovered to be downstream gene of miR-617, which is an important component of TGF-β signaling. Smad3 (mothers against decapentaplegic homolog 3) is a crucial regulator of TGF-β/ Smads pathway 41 . It is able to mediate the synthesis and degradation of extracellular matrix, as well as cell phenotypes 42,43 .…”

miR-129-3p alleviates chondrocyte apoptosis in knee joint fracture-induced osteoarthritis through CPEB1

“…According to the results, miR-129-3p overexpression rescued chondrocyte viability and impaired apoptosis and cleaved caspase-3 expression, and miR-129-3p inhibition presented the reverse function, unraveling the potential therapeutic effect of miR-129-3p on OA-induced chondrocyte apoptosis. miR-129-3p has been reported to be inhibited in palmitic acid-treated cardiomyocytes, and overexpression of miR-129-3p could ameliorate cardiomyocyte inflammation and apoptosis [ 13 ]. Moreover, CPEB1 silence markedly enhanced the cell viability and inhibited chondrocyte apoptosis.…”

“…miR-129-3p has also been mentioned in renal cell carcinoma as a promising diagnostic biomarker and a suppressor of multiple metastasis-related genes [ 11 ]. More importantly, the anti-apoptotic effect of miR-129-3p has been elucidated in cardiomyocytes and breast cancer cells [ 12 , 13 ]. miR-129-3p has also been confirmed to inhibit the expression of inflammatory cytokine IL-17 in rheumatoid arthritis [ 14 ].…”