tannins and Fibrosis

Several chemicals and medications induce cellular damage in various organs of the body by activating reactive substances' metabolism leading to various pathological conditions including liver disease. In this study, we evaluated the prophylactic and curative effects of Carica papaya Linn. pulp water extract (PE) against CCl

Topics: Animals; Antioxidants; Carbon Tetrachloride; Carica; Chemical and Drug Induced Liver Injury; Fibrosis; Flavonoids; Inflammation; Lipid Peroxidation; Liver; Male; Oxidative Stress; Plant Extracts; Rats; Tannins

Vocal fold fibrosis is an abnormal condition characterized by unfavorable changes in the organization of the extracellular matrix in vocal fold lamina propria. To prevent and treat vocal fold fibrosis, a number of synthetic drugs, such as mitomycin C and the glucocorticoid family, are used after surgery, but these are known to have some side effects. Therefore, using both in vitro and in vivo studies, this study investigated whether phlorotannins extracted from Ecklonia cava have the potential to prevent vocal fold fibrosis with minimal side effects. The results show that phlorotannins suppressed both the expression of the fibrotic phenotypic marker and cell migration by inhibiting the activation of the mitogen-activated protein kinase (MAPK) and Smad2/3 signaling pathways in human vocal fold fibroblasts stimulated by transforming growth factor-β. Additionally, phlorotannins exhibited antifibrotic efficacy without an excessive inflammatory response in a laser-induced fibrosis rabbit model when delivered as an aerosol via inhalation. Based on these results, phlorotannins should be considered a promising candidate for use in the prevention of vocal fold fibrosis.

Topics: Administration, Inhalation; Aerosols; Animals; Biomarkers; Cell Death; Cell Movement; Cell Survival; Disease Models, Animal; Endoscopy; Extracellular Matrix; Fibroblasts; Fibrosis; Humans; Lasers; Male; MAP Kinase Signaling System; Phenotype; Rabbits; Smad Proteins; Tannins; Transforming Growth Factor beta; Vocal Cords

Polarized macrophages induce fibrosis through multiple mechanisms, including a process termed epithelial-to-mesenchymal transition (EMT). Mesenchymal cells contribute to the excessive accumulation of fibrous connective tissues, leading to organ failure. This study was aimed to investigate the effect of tannic acid (TA), a natural dietary polyphenol on M1 macrophage-induced EMT and its underlying mechanisms.. First, we induced M1 polarization in macrophage cell lines (RAW 264.7 and THP-1). Then, the conditioned-medium (CM) from these polarized macrophages was used to induce EMT in the human adenocarcinomic alveolar epithelial (A549) cells. We also analysed the role of TA on macrophage polarization.. We found that TA pre-treated CM did not induce EMT in epithelial cells. Further, TA pre-treated CM showed diminished activation of MAPK in epithelial cells. Subsequently, TA was shown to inhibit LPS-induced M1 polarization in macrophages by directly targeting toll-like receptor 4 (TLR4), thereby repressing LPS binding to TLR4/MD2 complex and subsequent signal transduction.. It was concluded that TA prevented M1 macrophage-induced EMT by suppressing the macrophage polarization possibly through inhibiting the formation of LPS-TLR4/MD2 complex and blockage of subsequent downstream signal activation. Further, our findings may provide beneficial information to develop new therapeutic strategies against chronic inflammatory diseases.

Topics: A549 Cells; Animals; Anti-Inflammatory Agents; Epithelial-Mesenchymal Transition; Fibrosis; Humans; Lipopolysaccharides; Lung; Macrophage Activation; Mice; RAW 264.7 Cells; Tannins; THP-1 Cells; Toll-Like Receptor 4

In response to tissue injury, fibroblasts migrate into the wound, where they undergo proliferation and differentiation. The persistence of these differentiated fibroblasts (myofibroblasts) is associated with excessive scarring in various organs. We aimed to investigate the effects of Tannic acid (TA) on fibroblast proliferation and differentiation, and found that TA inhibited fibroblast differentiation as assessed by reduced expression of α-smooth muscle actin, N-cadherin, and type-1-collagen. TA also prevented the TGF-β1-induced alteration in the expression of two classes of genes involved in the remodeling of extracellular matrix (ECM) proteins, namely matrix metalloproteinases (Mmp-2 and -9) and tissue inhibitors of metalloproteinases (Timp-1 and -3). Further, TA suppressed TGF-β1-induced cell proliferation and induced cell cycle arrest at G0/G1 phase via targeting Cyclins expression. Finally, TA exerted its inhibitory effects by decreasing the phosphorylation of Smad and ERK signaling. In sum, our results suggesting that TA may be a potential therapeutic agent for pathological fibrosis.

Topics: Actins; Animals; Cadherins; Cell Differentiation; Collagen Type I; Extracellular Matrix; Fibrosis; G1 Phase; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Mice; Myofibroblasts; NIH 3T3 Cells; Resting Phase, Cell Cycle; Tannins; Transforming Growth Factor beta1

The aim of this study was to examine the cardioprotective effects and latent mechanism of tannic acid (TA) on cardiac hypertrophy.. Abdominal aortic banding (AAB) was used to induce pressure overload-induced cardiac hypertrophy in male Wistar rats, sham-operated rats served as controls. AAB rats were treated with TA (20 and 40 mg/kg) or captoril.. Tannic acid displayed obvious suppression of AAB-induced cardiac hypertrophy in rats. The cardioprotective effects of TA may be attributed to multitargeted inhibition of oxidative stress, inflammation, fibrosis and apoptosis in addition to an increase in NO levels, decrease in ET-1 levels, and downregulation of angiotensin receptors and the phosphorylation of ERK1/2.

Topics: Animals; Apoptosis; Captopril; Cardiomegaly; Cardiotonic Agents; Disease Models, Animal; Dose-Response Relationship, Drug; Down-Regulation; Endothelin-1; Fibrosis; Inflammation; Male; Nitric Oxide; Oxidative Stress; Rats; Rats, Wistar; Receptors, Angiotensin; Tannins