Effects of herbal extracts and compounds and pharmacological agents on pulmonary fibrosis in animal models: a review

Mojiri-Forushani, Hoda; Hemmati, Ali Asghar; Dehghani, Mohammad Amin; Malayeri, Alireza; Pour, Hossein Hassan

doi:10.1016/s2095-4964(17)60363-7

Cited by 13 publications

(6 citation statements)

References 44 publications

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“…Natural products and their derivatives have been used for the treatment of various diseases, including infectious diseases, and have been reported to serve an important role in the prevention of inflammatory diseases (13-15). It is well known that Traditional Chinese Medicine exerts valuable therapeutic effects on pulmonary diseases (16). Pistacia weinmannifolia (PW) is a plant predominantly distributed in the Yunnan province of China and is used as a herbal remedy for treating dysentery, enteritis, influenza and lung cancer (17,18).…”

Section: Introductionmentioning

confidence: 99%

Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide‑induced pulmonary inflammation by inhibiting interleukin‑8 production and NF‑κB activation

et al. 2019

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Pistacia weinmannifolia (PW) has been used in traditional Chinese medicine to treat headaches, dysentery, enteritis and influenza. However, PW has not been known for treating respiratory inflammatory diseases, including chronic obstructive pulmonary disease (COPD). The present in vitro analysis confirmed that PW root extract (PWRE) exerts anti-inflammatory effects in phorbol myristate acetate- or tumor necrosis factor α (TNF-α)-stimulated human lung epithelial NCI-H292 cells by attenuating the expression of interleukin (IL)-8, IL-6 and Mucin A5 (MUC5AC), which are closely associated with the pulmonary inflammatory response in the pathogenesis of COPD. Thus, the aim of the present study was to evaluate the protective effect of PWRE on pulmonary inflammation induced by cigarette smoke (CS) and lipopoly-saccharide (LPS). Treatment with PWRE significantly reduced the quantity of neutrophils and the levels of inflammatory molecules and toxic molecules, including tumor TNF-α, IL-6, IL-8, monocyte chemoattractant protein-1, neutrophil elastase and reactive oxygen species, in the bronchoalveolar lavage fluid of mice with CS- and LPS-induced pulmonary inflammation. PWRE also attenuated the influx of inflammatory cells in the lung tissues. Furthermore, PWRE downregulated the activation of nuclear factor-κB and the expression of phosphodiesterase 4 in the lung tissues. Therefore, these findings suggest that PWRE may be a valuable adjuvant treatment for COPD.

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Section: Introductionmentioning

confidence: 99%

Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide‑induced pulmonary inflammation by inhibiting interleukin‑8 production and NF‑κB activation

et al. 2019

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“…However, what is the molecular mechanism of AE against pulmonary fibrosis? Large amounts of evidence indicate that oxidative stress, inflammation and fibrosis are three key pathways involved in PF (Kolb et al, 2017; Mojiri‐Forushani et al, 2017; Selman et al, 2001). Hence, we explore these three pathways in order to elaborate molecular mechanism of AE against pulmonary fibrosis.…”

Section: Results and Disscussionmentioning

confidence: 99%

“…Although the etiology of IPF is not well understood, large amounts of study have reported that oxidative stress caused through Nrf pathway, inflammation caused through NF‐kB pathway and fibrosis caused through TGF‐beta1/Smad2/3 pathway are three key pathways in its initiation and deterioration (Kolb, Bonella, & Wollin, 2017; Mojiri‐Forushani, Hemmati, Dehghani, Malayeri, & Pour, 2017; Selman, King, & Pardo, 2001). Clinical studies have found a significant increase in lipid peroxides and inflammation in IPF patients, and the experimental animals suffered from pulmonary fibrosis have also demonstrated a positive correlation between the severity of pulmonary fibrosis and the state of oxidative stress and inflammation.…”

Section: Introductionmentioning

confidence: 99%

Arenaria kansuensis attenuates pulmonary fibrosis in mice via the activation of Nrf2 pathway and the inhibition of NF‐kB/TGF‐beta1/Smad2/3 pathway

Cui

Xin

Tao

et al. 2020

Phytotherapy Research

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Pulmonary fibrosis is a key feature of COVID‐19, Chinese herbal medicine Arenaria kansuensis has been used for curing pulmonary disease and antivirus for a long time and it has the potential against COVID‐19. In this work, protective effect of A. kansuensis ethanol extract (AE) on pulmonary fibrosis was evaluated through paraquat (PQ)‐induced pulmonary fibrosis animal model. Results showed that AE could significantly improve the survival rate, increase the body weight and reduce the lung index of mice at the raw drug doses of 700 and 350 mg/kg. Histopathological observation results showed that the destruction degree of lung tissue structure in mice was significantly improved with the increase of AE dosage. Collagen deposition in lung interstitium was significantly reduced. The marker protein alpha‐SMA involved in PF were significantly inhibited through repressing TGF‐beta1/Smads pathway. The degree of inflammatory infiltration was significantly reduced and inflammatory cytokines were significantly inhibited in mice through inhibiting the NF‐kB‐p65. Besides, oxidant stress level including upregulated ROS and down‐regulated SOD and GSH was efficiently improved by AE through upregulation of Nrf2 and downregulation of NOX4. In summary, this study firstly showed that the protective effect of AE on pulmonary fibrosis was partly due to activation of Nrf2 pathway and the inhibition of NF‐kB/TGF‐beta1/Smad2/3 pathway.

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“…Pulmonary fibrosis (PF) is defined as a progressive lung injury disease with unknown pathogeny, which is characterized by aberrant proliferation of fibroblasts, damage of alveolar epithelial cell, and excessive collagen accumulation [1,2]. The 4-year risk of death with PF is almost 41.0% [3].…”

Section: Introductionmentioning

confidence: 99%

Buyang Huanwu Tang inhibits cellular epithelial-to-mesenchymal transition by inhibiting TGF-β1 activation of PI3K/Akt signaling pathway in pulmonary fibrosis model in vitro

Yin

Wei

Wang

et al. 2020

BMC Complement Med Ther

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Background: Pulmonary fibrosis (PF) is a chronic and progressive interstitial lung disease. Buyang Huanwu Tang (BYHWT), a classical traditional Chinese medicine formula, has been widely utilized for the treatment of PF in China. This present study aimed to explore the mechanism of BYHWT in the treatment of PF in vitro. Methods: TGF-β1 stimulated human alveolar epithelial A549 cells were used as in vitro model for PF. Post the treatment of BYHWT, cell viability was measured by MTT assay, and cell morphology was observed under microscope. The epithelial-to-mesenchymal transition (EMT) markers (E-cadherin, Vimentin) and collagen I (Col I) were detected by western blot, immunofluorescence staining and real-time quantitative polymerase chain reaction. With the co-administration of activators (IGF-1, SC79) and inhibitors (LY294002, MK2206), the effect of BYHWT on PI3K/Akt pathway was analyzed by western blot. Results: BYHWT inhibited cell growth, and prevented cell morphology changed from epithelial to fibroblasts in TGF-β1 induced A549 cells. BYHWT decreased Vimentin and Col I, while increased E-cadherin at both protein and mRNA levels. Moreover, phosphorylation of PI3K (p-PI3K) and phosphorylation of Akt (p-Akt) were significantly down-regulated by BYHWT in TGF-β1 stimulated A549 cells. Conclusion:These results indicate that BYHWT suppressed TGF-β1-induced collagen accumulation and EMT of A549 cells by inhibiting the PI3K/Akt signaling pathway. These findings suggest that BYHWT may have potential for the treatment of PF.

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Effects of herbal extracts and compounds and pharmacological agents on pulmonary fibrosis in animal models: a review

Cited by 13 publications

References 44 publications

Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide‑induced pulmonary inflammation by inhibiting interleukin‑8 production and NF‑κB activation

Pistacia weinmannifolia ameliorates cigarette smoke and lipopolysaccharide‑induced pulmonary inflammation by inhibiting interleukin‑8 production and NF‑κB activation

Arenaria kansuensis attenuates pulmonary fibrosis in mice via the activation of Nrf2 pathway and the inhibition of NF‐kB/TGF‐beta1/Smad2/3 pathway

Buyang Huanwu Tang inhibits cellular epithelial-to-mesenchymal transition by inhibiting TGF-β1 activation of PI3K/Akt signaling pathway in pulmonary fibrosis model in vitro

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