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Upregulation of miR‑335 exerts protective effects against sepsis‑induced myocardial injury.

ABSTRACT: Septicemia is associated with excessive inflammation, oxidative stress and apoptosis, causing myocardial injury that results in high mortality and disability rates worldwide. The abnormal expression of multiple microRNAs (miRNAs/miRs) is associated with more severe sepsis‑induced myocardial injury (SIMI) and miR‑335 has been shown to protect cardiomyocytes from oxidative stress. The present study aimed to investigate the role of miR‑335 in SIMI. An SIMI model was established by cecal ligation and puncture (CLP) in mice. An miRNA‑335 precursor (pre‑miR‑335) was transfected to accelerate miR‑335 expression and an miR‑335 inhibitor (anti‑miR‑335) was used to inhibit miR‑335 expression. CLP or sham surgery was performed on pre‑miR‑335, anti‑miR‑335 and wild‑type mice and miR‑335 expression was determined by reverse transcription‑quantitative PCR. Inflammatory factors (TNF‑α, IL‑6 and IL‑10) and troponin (cTNI), brain natriuretic peptide (BNP), creatine kinase (CK), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) were assessed using commercial kits. Apoptosis was detected by flow cytometry and cardiac function was assessed using a Langendorff isolated cardiac perfusion system. miR‑335 expression was upregulated and an elevation in inflammatory factors and cTNI, BNP, CK, LDH and AST was observed. Compared with the wild‑type control group, pre‑miR‑335 mice treated with CLP exhibited significantly reduced left ventricular development pressure, maximum pressure increased reduction rates, as well as decreased levels of TNF‑α, IL‑6 and IL‑10, myocardial injury and apoptosis; by contrast, these features were amplified in CLP‑treated anti‑miR‑335 mice. In conclusion, the upregulation of miR‑335 exerted ameliorative effects on myocardial injury following sepsis and may indicate a novel therapeutic intervention for SIMI.

SUBMITTER: Long X

PROVIDER: S-EPMC8477184 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Inhalation of crystalline silica particles leads to pulmonary fibrosis, eventually resulting in respiratory failure and death. There are few effective drugs that can delay the progression of this disease; thus, patients with silicosis are usually only offered supportive care. Dioscin, a steroidal saponin, exhibits many biological activities and health benefits including its protective effects against hepatic fibrosis. However, the effect of dioscin on silicosis is unknown.We employed experimental mouse mode of silicosis. Different doses of dioscin were gavaged to the animals 1 day after crystalline silica instillation to see the effect of dioscin on crystalline silica induced pulmonary fibrosis. Also, we used RAW264.7 and NIH-3T3 cell lines to explore dioscin effects on macrophages and fibroblasts. Dioscin was also oral treatment but 10 days after crystalline silica instillation to see its effect on established pulmonary fibrosis.Dioscin treatment reduced pro-inflammation and pro-fibrotic cytokine secretion by modulating innate and adaptive immune responses. It also reduced the recruitment of fibrocytes, protected epithelial cells from crystalline silica injury, inhibited transforming growth factor beta/Smad3 signaling and fibroblast activation. Together, these effects delayed the progression of crystalline silica-induced pulmonary fibrosis. The mechanism by which dioscin treatment alleviated CS-induced inflammation appeared to be via the reduction of macrophage, B lymphocyte, and T lymphocte infiltration into lung. Dioscin inhibits macrophages and fibroblasts from secreting pro-inflammatory cytokines and may also function as a modulator of T helper cells responses, concurrent with attenuated phosphorylation of the apoptosis signal-regulating kinase 1-p38/c-Jun N-terminal kinase pathway. Also, dioscin could block the phosphorylation of Smad3 in fibroblast. Oral treatment of dioscin could also effectively postpone the progression of established silicosis.Oral treatment dioscin delays crystalline silica-induced pulmonary fibrosis and exerts pulmonary protective effects in mice. Dioscin may be a novel and potent candidate for protection against crystalline silica-induced pulmonary fibrosis.

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Upregulation of miR‑335 exerts protective effects against sepsis‑induced myocardial injury.

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