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  • br Conclusions In summary KLA isolated

    2022-12-09


    Conclusions In summary, KLA isolated from K. senegalensis exerted the anti-inflammatory activity via inhibiting the activation of NF-κB, AP-1, AKT and upregulating p38 MAPK/Nrf2/HO-1 signaling in LPS-stimulated RAW 264.7 and BV-2 LRRK2-IN-1 receptor (Fig. 9). These properties provide a potential mechanism that explains the anti-inflammatory activity of KLA.
    Conflict of interest
    Acknowledgments This research was supported in part by the National Natural Science Foundation of China (31470416), the program for New Century Excellent Talents in University (NCET-2013-1015), the Outstanding Youth Fund of the Basic Research Program of Jiangsu Province (BK20160077), the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD), and the Ph.D. Programs Foundation of Ministry of Education of China (20120096130002).
    Introduction Pulmonary fibrosis (PF), a common chronic lung disease, is characterized by restrictive functional ventilatory disturbance, hypoxemia, and chronic progressive diffuse pulmonary fibrosis, and its clinical manifestations include wheezing, difficulty breathing, and dry coughs, which leads to high morbidity and mortality around the world [1]. So far, the pathogenesis of PF is not fully understood [2,3], thus no effective medication or satisfactory therapy has been developed. Resveratrol (Res) is a type of polyphenolic compound that has many biological activities, including anti-aging, anti-oxidation, anti-inflammation, anti-tumor activity, anti-platelet aggregation, mediation of cell apoptosis, regulation of estrogen, and immunity [4]. The antioxidant activity of Res enables it to mitigate oxidative damage and fibrosis, which exerts in vivo protection against pulmonary fibrosis [5]. For example, Res can prohibit the pathologic progress of PF in bleomycin (BLM)-induced animal models [6]. In vitro, resveratrol inhibits the proliferation and differentiation of lung fibroblasts, as well as reduces the deposition of extracellular collagen [7]. However, the molecular mechanisms involving Res in the occurrence and development of PF remain unknown. MicroRNAs (miRNAs) are a class of endogenous non-coding single-stranded small RNA molecules with a length of 22 nucleotides that block protein synthesis and negatively regulate gene expression at the post-transcriptional level by binding to complementary mRNA sequences in the 3′-untranslated region of target genes. MiRNAs have been implicated in the physiological and pathological processes of PF [8,9]. Therefore, confirming the specific roles of miRNAs in the pathogenesis of PF is developing as a novel research direction for PF therapy. MicroRNA-21 (miR-21) has been shown to be associated with the development of lung fibrosis in numerous studies. For instance, Liu et al. [8] reported that miR-21 is aberrantly upregulated in the lung tissues of mice with pulmonary fibrosis and that reducing miR-21 levels efficiently alleviates the severity of BLM-induced lung fibrosis and myofibroblast differentiation. An increase of miR-21 levels in primary lung fibroblasts promotes fibrosis-related responses including fibroblast activation and collagen deposition by regulating TGF-β1 expression, whereas the silencing of miR-21 alleviates fibrosis symptoms efficiently [8]. In addition, the important function of miR-21 in PF pathogenesis has been proposed to exert through regulation of the TGF-β1/Smad signaling pathways and related downstream genes [10]. Numerous studies have shown that resveratrol plays an inhibitory role in the growth and metastasis of neoplasm by downregulating miR-21 [[11], [12], [13]]. In addition, Res attenuates myocardial fibrosis and ameliorates myocardial remodeling or ischemia via the down-regulation of miR-21 [14]. However, whether the positive effect of resveratrol on pulmonary fibrosis is associated with miR-21 has not been fully explored. In the present study, we established a pulmonary fibrosis animal model using BLM and observed the effects of changes of miR-21 levels by treatment with Res and/or miR-21 agomir. We also detected the expression of the promoter regions of miR-21 and assessed the potential regulatory relationship between Res and miR-21. In brief, our study identifies the potential role of miR-21 in the development of PF, as well as the corresponding molecular mechanism, which provides a theoretical basis for the clinical application of Res in treating pulmonary fibrosis.