Publications by authors named "Ayyanar Sivanantham"

10 Publications

  • Page 1 of 1

Anti-asthmatic effects of tannic acid from Chinese natural gall nuts in a mouse model of allergic asthma.

Int Immunopharmacol 2021 Jun 11;98:107847. Epub 2021 Jun 11.

Department of Biochemistry, ICMR-National Institute for Research in Environmental Health, Bhopal, Madhya Pradesh, India. Electronic address:

Asthma is a chronic inflammatory disease of the airways, which is characterized by infiltration of inflammatory cells, airway hyperresponsiveness (AHR), and airway remodeling. This study aimed to explore the role and mechanism of tannic acid (TA), a naturally occurring plant-derived polyphenol, in murine asthma model. BALB/c mice were given ovalbumin (OVA) to establish an allergic asthma model. The results revealed that TA treatment significantly decreased OVA-induced AHR, inflammatory cells infiltration, and the expression of various inflammatory mediators (Th2 and Th1 cytokines, eotaxin, and total IgE). Additionally, TA treatment also attenuated increases in mucins (Muc5ac and Muc5b) expression, mucus production in airway goblet cells, mast cells infiltration, and airway remodeling induced by OVA exposure. Furthermore, OVA-induced NF-κB (nuclear factor- kappa B) activation and cell adhesion molecules expression in the lungs was suppressed by TA treatment. In conclusion, TA effectively attenuated AHR, inflammatory response, and airway remodeling in OVA-challenged asthmatic mice. Therefore, TA may be a potential therapeutic option against allergic asthma in clinical settings.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.intimp.2021.107847DOI Listing
June 2021

An overview on the role of plant-derived tannins for the treatment of lung cancer.

Phytochemistry 2021 May 8;188:112799. Epub 2021 May 8.

Department of Biochemistry, ICMR-National Institute for Research in Environmental Health, Bhopal, Madhya Pradesh, India. Electronic address:

Lung cancer is the leading cause of cancer-related death globally. Despite many advanced approaches to treat cancer, they are often ineffective due to resistance to classical anti-cancer drugs and distant metastases. Currently, alternative medicinal agents derived from plants are the major interest due to high bioavailability and fewer adverse effects. Tannins are polyphenolic compounds existing as specialized products in a wide variety of vegetables, fruits, and nuts. Many tannins have been found to possess protective properties, such as anti-inflammatory, anti-fibrotic, anti-microbial, anti-diabetic, and so on. This review aims to summarize the current knowledge addressing the anti-cancer effects of dietary tannins and their underlying molecular mechanisms. In vivo and in vitro studies provide evidences that anti-cancer effects of various tannins are predominantly mediated through negative regulation of transcription factors, growth factors, receptor kinases, and many oncogenic molecules. In addition, we also discussed the absorption, distribution, metabolism, excretion, and toxicity (ADMET) properties of tannins, clinical trial results as well as our perspective on future research with tannins.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.phytochem.2021.112799DOI Listing
May 2021

Therapeutic potential of plant-derived tannins in non-malignant respiratory diseases.

J Nutr Biochem 2021 Aug 29;94:108632. Epub 2021 Mar 29.

Department of Biotechnology, BIT-Campus, Anna University, Tiruchirappalli, Tamil Nadu, India.

Respiratory diseases are the major cause of human illness and death around the world. Despite advances in detection and treatment, very few classes of safe and effective therapy have been introduced to date. At present, phytochemicals are getting more attention because of their diverse beneficial activities and minimal toxicity. Tannins are polyphenolic secondary metabolites with high molecular weights, which are naturally present in a wide variety of fruits, vegetables, cereals, and leguminous seeds. Many tannins are endowed with well-recognized protective properties, such as anti-cancer, anti-microbial, anti-oxidant, anti-hyperglycemic, and many others. This review summarizes a large body of experimental evidence implicating that tannins are helpful in tackling a wide range of non-malignant respiratory diseases including acute lung injury (ALI), pulmonary fibrosis, asthma, pulmonary hypertension, and chronic obstructive pulmonary disease (COPD). Mechanistic pathways by which various classes of tannins execute their beneficial effects are discussed. In addition, clinical trials and our perspective on future research with tannins are also reviewed.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jnutbio.2021.108632DOI Listing
August 2021

Tannic acid alleviates experimental pulmonary fibrosis in mice by inhibiting inflammatory response and fibrotic process.

Inflammopharmacology 2020 Oct 5;28(5):1301-1314. Epub 2020 May 5.

Department of Biotechnology, BIT-Campus, Anna University, Tiruchirappalli, Tamil Nadu, 620024, India.

Pulmonary fibrosis (PF) is a chronic and irreversible scarring disease in the lung with limited treatment options. Therefore, it is critical to identify new therapeutic options. This study was undertaken to identify the effects of tannic acid (TA), a naturally occurring dietary polyphenol, in a mouse model of PF. Bleomycin (BLM) was intratracheally administered to induce PF. Administration of TA significantly reduced BLM-induced histological alterations, inflammatory cell infiltration and the levels of various inflammatory mediators (nitric oxide, leukotriene B and cytokines). Additionally, treatment with TA also impaired BLM-mediated increases in pro-fibrotic (transforming growth factor-β1) and fibrotic markers (alpha-smooth muscle actin, vimentin, collagen 1 alpha and fibronectin) expression. Further investigation indicated that BLM-induced phosphorylation of Erk1/2 (extracellular signal-regulated kinases 1 and 2) in lungs was suppressed by TA treatment. Findings of this study suggest that TA has the potential to mitigate PF through inhibiting the inflammatory response and fibrotic process in lungs and that TA might be useful for the treatment of PF in clinical practice.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10787-020-00707-5DOI Listing
October 2020

Tannic acid prevents macrophage-induced pro-fibrotic response in lung epithelial cells via suppressing TLR4-mediated macrophage polarization.

Inflamm Res 2019 Dec 5;68(12):1011-1024. Epub 2019 Sep 5.

Department of Biotechnology, BIT-Campus, Anna University, Tiruchirappalli, Tamil Nadu, India.

Background: 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.

Materials: 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.

Results: 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.

Conclusion: 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.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00011-019-01282-4DOI Listing
December 2019

Tannic acid protects against experimental acute lung injury through downregulation of TLR4 and MAPK.

J Cell Physiol 2019 05 24;234(5):6463-6476. Epub 2018 Sep 24.

Department of Biotechnology, BIT-Campus, Anna University, Tiruchirappalli, India.

Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) remain a major cause of morbidity and mortality in critically ill patients, and no specific therapies are still available to control the mortality rate. Thus, we explored the preventive and therapeutic effects of tannic acid (TA), a natural polyphenol in the context of ALI. We used in vivo and in vitro models, respectively, using lipopolysaccharide (LPS) to induce ALI in mice and exposing J774 and BEAS-2B cells to LPS. In both preventive and therapeutic approaches, TA attenuated LPS-induced histopathological alterations, lipid peroxidation, lung permeability, infiltration of inflammatory cells, and the expression of proinflammatory mediators. In addition, in-vitro study showed that TA treatment could reduce the expression of proinflammatory mediators. Further studies revealed that TA-dampened inflammatory responses by downregulating the LPS-induced toll-like receptor 4 (TLR4) expression and inhibiting extracellular-signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) activation. Furthermore, cells treated with the inhibitors of ERK1/2 (PD98059) and p38 (SB203580) mitigated the expression of cytokines induced by LPS, thus suggesting that ERK1/2 and p38 activity are required for the inflammatory response. In conclusion, TA could attenuate LPS-induced inflammation and may be a potential therapeutic agent for ALI-associated inflammation in clinical settings.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jcp.27383DOI Listing
May 2019

Tannic acid modulates fibroblast proliferation and differentiation in response to pro-fibrotic stimuli.

J Cell Biochem 2018 08 17;119(8):6732-6742. Epub 2018 Apr 17.

Department of Biotechnology, Anna University, BIT-Campus, Tiruchirappalli, Tamil Nadu, India.

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.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jcb.26866DOI Listing
August 2018

Tannic acid attenuates TGF-β1-induced epithelial-to-mesenchymal transition by effectively intervening TGF-β signaling in lung epithelial cells.

J Cell Physiol 2018 Mar 30;233(3):2513-2525. Epub 2017 Aug 30.

Department of Biotechnology, Anna University, BIT-Campus, Tiruchirappalli, Tamil Nadu, India.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and an irreversible lung disorder characterized by the accumulation of fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor-β1 (TGF-β1)-induced epithelial-to-mesenchymal transition (EMT) is thought to be one of the possible sources for a substantial increase in the number of fibroblasts/myofibroblasts in IPF lungs. Tannic acid (TA), a natural dietary polyphenolic compound has been shown to possess diverse pharmacological effects. However, whether TA can inhibit TGF-β1-mediated EMT in lung epithelial cells remains enigmatic. Both the human adenocarcinomic alveolar epithelial (A549) and normal bronchial epithelial (BEAS-2B) cells were treated with TGF-β1 with or without TA. Results showed that TA addition, markedly inhibited TGF-β1-induced EMT as assessed by reduced expression of N-cadherin, type-1-collagen, fibronectin, and vimentin. Furthermore, TA inhibited TGF-β1-induced cell proliferation through inducing cell cycle arrest at G0/G1 phase. TGF-β1-induced increase in the phosphorylation of Smad (Smad2 and 3), Akt as well as that of mitogen activated protein kinase (ERK1/2, JNK1/2, and p38) mediators was effectively inhibited by TA. On the other hand, TA reduced the TGF-β1-induced increase in TGF-β receptors expression. Using molecular docking approach, FTIR, HPLC and Western blot analyses, we further identified the direct binding of TA to TGF-β1. Finally, we conclude that TA might directly interact with TGF-β1, thereby repressing TGF-β signaling and subsequent EMT process in lung epithelial cells. Further animal studies are needed to clarify its potential therapeutic benefit in pulmonary fibrosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jcp.26127DOI Listing
March 2018

C-phycocyanin suppresses transforming growth factor-β1-induced epithelial mesenchymal transition in human epithelial cells.

Pharmacol Rep 2017 May 5;69(3):426-431. Epub 2017 Jan 5.

Department of Biotechnology, Anna University, BIT-Campus, Tiruchirappalli, Tamil Nadu, India.

Background: Epithelial mesenchymal transition (EMT) is a process through which epithelial cells undergo multiple biochemical changes, causing them to differentiate into a mesenchymal-cell phenotype. This process has been shown to contribute to the development of fibrotic diseases. C-phycocyanin (C-PC) is a phycobiliprotein extracted from Spirulina platensis. This study was done to investigate the effect of C-PC on transforming growth factor-β1 (TGF-β1)-induced EMT and an EMT associated proliferation in human epithelial cell lines.

Methods: Human adenocarcinoma cell line, A549 and breast cancer cell line, MCF-7 were treated with TGF-β1, and EMT-related genes expression, cell proliferation and cell cycle arrest were examined.

Results: C-PC suppressed the EMT as assessed by reduced expression of vimentin, type-1-collagen and fibronectin, and increased E-cadherin expression in TGF-β1 treated cells. Further, TGF-β1 treatment induced cell cycle arrest in S and G2/M phase in A549 cells. However, TGF-β1-mediated cell cycle arrest was significantly reversed by combined treatment with C-PC.

Conclusions: The overall data suggested that C-PC suppresses TGF- β1-induced EMT and warrants further in vivo studies for future evaluation of C-PC as a potential antifibrotic agent.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.pharep.2016.12.013DOI Listing
May 2017

C-phycocyanin suppresses transforming growth factor-β1-induced epithelial mesenchymal transition in human epithelial cells.

Pharmacol Rep 2017 Jun 5;69(3):426-431. Epub 2017 Jan 5.

Department of Biotechnology, Anna University, BIT-Campus, Tiruchirappalli, Tamil Nadu, India. Electronic address:

Background: Epithelial mesenchymal transition (EMT) is a process through which epithelial cells undergo multiple biochemical changes, causing them to differentiate into a mesenchymal-cell phenotype. This process has been shown to contribute to the development of fibrotic diseases. C-phycocyanin (C-PC) is a phycobiliprotein extracted from Spirulina platensis. This study was done to investigate the effect of C-PC on transforming growth factor-β1 (TGF-β1)-induced EMT and an EMT associated proliferation in human epithelial cell lines.

Methods: Human adenocarcinoma cell line, A549 and breast cancer cell line, MCF-7 were treated with TGF-β1, and EMT-related genes expression, cell proliferation and cell cycle arrest were examined.

Results: C-PC suppressed the EMT as assessed by reduced expression of vimentin, type-1-collagen and fibronectin, and increased E-cadherin expression in TGF-β1 treated cells. Further, TGF-β1 treatment induced cell cycle arrest in S and G2/M phase in A549 cells. However, TGF-β1-mediated cell cycle arrest was significantly reversed by combined treatment with C-PC.

Conclusions: The overall data suggested that C-PC suppresses TGF- β1-induced EMT and warrants further in vivo studies for future evaluation of C-PC as a potential antifibrotic agent.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.pharep.2016.12.013DOI Listing
June 2017