Berberine inhibits Smad and non-Smad signaling cascades and enhances autophagy against pulmonary fibrosis

Palanivel, Chitra; Gowrikumar, Saiprasad; Manikandan, R.; Sudhandiran, Ganapasam

doi:10.1007/s00109-015-1283-1

Cited by 87 publications

(62 citation statements)

References 34 publications

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“…More recently, it was reported that BBR could alleviate high glucose-induced podocyte apoptosis via autophagy 15 . In addition, BBR can stimulate autophagy in various tissues including heart 16 , lungs 17 and hepar 18 , however, this has not been shown in the NP. Considering that oxidative stress, apoptosis and inflammatory activation are all elements of IVDD pathology, we hypothesize that BBR may utilize autophagy to prevent the formation of IVDD.…”

Section: Introductionmentioning

confidence: 92%

Berberine suppresses apoptosis and extracellular matrix (ECM) degradation in nucleus pulposus cells and ameliorates disc degeneration in a rodent model

et al. 2018

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Intervertebral disc degeneration (IVDD) is a chronic disease with complicated pathology involving nucleus pulposus (NP) cell apoptosis and extracellular matrix (ECM) degradation. Previous studies have shown that moderate autophagy has a protective effect against apoptosis in NP cells. Berberine (BBR) is an alkaloid compound with many beneficial properties including antimicrobial, anti-inflammatory, antioxidative, and anti-apoptotic activity. Recently, it was found to induce autophagy in various tissues as well. Thus, we hypothesized that BBR may exert a therapeutic effect on IVDD through autophagy activation. In this study, we investigated the effects of BBR on IVDD and delineated a potential mechanism. BBR treatment in vitro inhibited the expression of pro-apoptotic proteins induced by tert-butyl hydroperoxide (TBHP), and increased the expression of anti-apoptotic Bcl-2. Furthermore, it prevented ECM degradation by inhibiting the production of matrix-degrading enzymes. Additionally, BBR treatment significantly activated autophagy in NP cells. However, autophagy inhibition markedly suppressed BBR's effects on NP cell apoptosis and ECM degeneration, indicating that autophagy activation with BBR treatment is protective against IVDD. In vivo, BBR treatment increased the expression of LC3 in disc cells and prevented the development of IVDD in a needle puncture-induced rat model. Thus, BBR stimulates autophagy as a protective mechanism against NP cell apoptosis and ECM degeneration, revealing its therapeutic potential in the treatment of IVDD.

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Section: Introductionmentioning

confidence: 92%

Berberine suppresses apoptosis and extracellular matrix (ECM) degradation in nucleus pulposus cells and ameliorates disc degeneration in a rodent model

et al. 2018

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“…16,17 All rats were sutured with amikacin lotion at the neck suture 3 days post-operation. Rats were divided into different groups: normal group (15 normal rats), control group (30 rats injected with saline), and BLM group (110 rats injected with 40 mg/kg sodium pentobarbital).…”

Section: Animal Treatmentmentioning

confidence: 99%

Protective effect of bicyclol against pulmonary fibrosis via regulation of microRNA‐455‐3p in rats

Zhou

Chai

2019

J of Cellular Biochemistry

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Idiopathic pulmonary fibrosis (IPF), a chronic, progressive and irreversible disease, needs long‐term treatment. Bicyclol was found to play a great role in pulmonary fibrosis, and the present study is to explore how bicyclol affects IPF with the involvement of microRNA‐455‐3p (miR‐455‐3p) and Bax. Bleomycin (BLM) was used to induce the IPF model in Sprague‐Dawley rats to detect the expression of miR‐455‐3p, Bax, and B‐cell lymphoma factor 2 (Bcl‐2). Moreover, to further investigate the mechanisms of bicyclol, the BLM‐induced fibrotic cell model was used after the lung epithelial cells HPAEpiC received miR‐455‐3p knockout treatment. The rats were then treated with vehicle and bicyclol, respectively. The apoptosis of fibrotic cells and Bax/Bcl‐2 were identified. Inhibition function of bicyclol was optimal at a dose of 150 mg/kg. Bicyclol inhibited cell apoptosis and reduced Bax/Bcl‐2 expression in rats. miR‐455‐3p could potentially bind to Bax gene. Bicyclol reduced the levels of methylenedioxyamphetamine, superoxide dismutase, and glutathione in rat lung tissue, inhibited the apoptosis of rats with IPF and upregulated miR‐455‐3p expression. In vitro studies showed that bicyclol significantly promoted miR‐455‐3p expression in HPAEpiC fibrosis. Bicyclol inhibited fibrosis‐induced apoptosis of HPAEpiC in alveolar epithelial cells through promoting miR‐455‐3p, which inhibited Bax expression in IPF. Bicyclol may suppress the apoptosis of alveolar epithelial cells by upregulating miR‐455‐3p. This study laid a theoretical foundation for further understanding of IPF and searching for new molecular therapeutic targets.

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“…Researchers have proved that C. sinensis can ameliorate fibrosis in the liver, pulmonary and kidney through inhibition of TGF-b1 expression and promotion of collagen degradation. 14,15 The growth of C. sinensis natural fungus is unusual owing to its limited ability to grow on Tibetan plateau and southwestern China. Hence, Hirsutella sinensis culturing in vitro became an attractive substitute for the preparation of health supplements.…”

Section: Introductionmentioning

confidence: 99%

Anti-fibrosis effect for Hirsutella sinensis mycelium based on inhibition of mTOR p70S6K phosphorylation

et al. 2017

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Hirsutella sinensis, cultured in vitro, is an attractive substitute for Cordyceps sinensis as health supplement. The aim of this study was to demonstrate whether H. sinensis mycelium (HSM) attenuates murine pulmonary fibrosis induced by bleomycin and to explore the underlying molecular mechanisms. Using lung fibrosis modle induced by intratracheal instillation of bleomycin (BLM; 4 mg/kg), we observed that the administration of HSM reduced HYP, TGF-β1 and the production of several pro-fibrosis cytokines (α-smooth muscle actin, fibronectin and vimentin) in fibrotic mice lung sections. Histopathological examination of lung tissues also demonstrated that HSM improved BLM-induced pathological damage. Concurrently, HSM supplementation markedly reduced the chemotaxis of alveolar macrophages and potently suppressed the expression of inflammatory cytokines. Also, HSM influenced Th1/Th2 and Th17/Treg imbalance and blocked the phosphorylation of mTOR pathway in vivo. Alveolar epithelial A549 cells acquired a mesenchymal phenotype and an increased expression of myofibroblast markers of differentiation (vimentin and fibronectin) after treatment with TGF-β1. HSM suppressed these markers and blocked the phosphorylation of mTOR pathway in vitro. The results provide evidence supporting the use of HSM in the intervention of pulmonary fibrosis and suggest that HSM is a potential therapeutic agent for lung fibrosis.

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Berberine inhibits Smad and non-Smad signaling cascades and enhances autophagy against pulmonary fibrosis

Cited by 87 publications

References 34 publications

Berberine suppresses apoptosis and extracellular matrix (ECM) degradation in nucleus pulposus cells and ameliorates disc degeneration in a rodent model

Berberine suppresses apoptosis and extracellular matrix (ECM) degradation in nucleus pulposus cells and ameliorates disc degeneration in a rodent model

Protective effect of bicyclol against pulmonary fibrosis via regulation of microRNA‐455‐3p in rats

Anti-fibrosis effect for Hirsutella sinensis mycelium based on inhibition of mTOR p70S6K phosphorylation

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