Asiatic acid inhibits pulmonary inflammation induced by cigarette smoke

Lee, Jae Won; Park, Hyun Ah; Kwon, Ok‐Kyoung; Jang, Yin-Gi; Kim, Ju Yeong; Choi, Bo Kyung; Lee, Hee Jae; Lee, Sang‐Woo; Paik, Jin‐Hyub; Oh, Sei‐Ryang; Ahn, Ki Hoon; Lee, Hyun Jun

doi:10.1016/j.intimp.2016.07.010

Cited by 53 publications

(33 citation statements)

References 93 publications

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“…Asiatic acid (AA) (Figure 1A) is a pentacyclic triterpene that widely occurs in many vegetables and fruits and has been reported to possess a variety of biological activities, including antioxidant and anti-inflammatory properties (19, 20). AA has been reported to reduce the pulmonary inflammation induced by cigarette smoking and inhibit liver fibrosis by blocking TGF-beta/Smad signaling in vivo and in vitro (21, 22). In this study, we explored whether AA attenuation of LPS/ d -GalN-induced hepatotoxicity was associated with the induction of AMPK/GSK3β-Nrf2 and PDCD4.…”

Section: Introductionmentioning

confidence: 99%

Asiatic Acid Exhibits Anti-inflammatory and Antioxidant Activities against Lipopolysaccharide and d-Galactosamine-Induced Fulminant Hepatic Failure

Wang

et al. 2017

Front. Immunol.

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Inflammation and oxidative stress are essential for the pathogenesis of fulminant hepatic failure (FHF). Asiatic acid (AA), which is a pentacyclic triterpene that widely occurs in various vegetables and fruits, has been reported to possess antioxidant and anti-inflammatory properties. In this study, we investigated the protective effects of AA against lipopolysaccharide (LPS) and d-galactosamine (GalN)-induced FHF and the underlying molecular mechanisms. Our findings suggested that AA treatment effectively protected against LPS/d-GalN-induced FHF by lessening the lethality; decreasing the alanine transaminase and aspartate aminotransferase levels, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α production, malondialdehyde formation, myeloperoxidase level and reactive oxygen species generation (i.e., H2O2, NO, and O2−), and increasing the glutathione and superoxide dismutase contents. Moreover, AA treatment significantly inhibited mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathway activation via the partial induction of programmed cell death 4 (PDCD4) protein expressions, which are involved in inflammatory responses. Furthermore, AA treatment dramatically induced the expression of the glutamate-cysteine ligase modifier subunit, the glutamate-cysteine ligase catalytic subunit, heme oxygenase-1, and NAD (P) H: quinoneoxidoreductase 1 (NQO1), which are largely dependent on activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2) through the induction of AMP-activated protein kinase (AMPK) and glycogen synthase kinase-3β (GSK3β) phosphorylation. Accordingly, AA exhibited protective roles against LPS/d-GalN-induced FHF by inhibiting oxidative stress and inflammation. The underlying mechanism may be associated with the inhibition of MAPK and NF-κB activation via the partial induction of PDCD4 and upregulation of Nrf2 in an AMPK/GSK3β pathway activation-dependent manner.

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Section: Introductionmentioning

confidence: 99%

Asiatic Acid Exhibits Anti-inflammatory and Antioxidant Activities against Lipopolysaccharide and d-Galactosamine-Induced Fulminant Hepatic Failure

Wang

et al. 2017

Front. Immunol.

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“…Asiatic acid (AA), a pentacyclic triterpene isolated from various plants including Centella asiatica, has shown anti-in ammation effect in many in ammatory conditions. Researchers found out that AA has bene cial effects in preventing in ammation occurred within lung or liver through down-regulating TGF-beta/Smad or NF-κB signaling pathway, respectively [20] [21]. People also found out that AA could ameliorate dextran sodium-induced murine experimental colitis [22], attenuated kainic-induced seizure by inhibiting hippocampal in ammatory and oxidative stress [23], and lipopolysaccharide-induced in ammation in human corneal epithelial cells [24].…”

Section: Introductionmentioning

confidence: 99%

Asiatic Acid Attenuates Osteoarthritis by Regulating NF-κB Signaling Pathway in Chondrocytes

Yang

Zhang

et al. 2020

Preprint

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Background: Natural small molecules have become more attractive as alternatives to non-steroidal anti-inflammatory drugs in osteoarthritis (OA) treatments. This study aims to investigate the effects of Asiatic acid (AA) on OA in chondrocytes and the surgery-induced OA animal model. Methods: Cytotoxicity of AA in primary rat articular chondrocytes was determined. Chondrocytes were pretreated with AA at the safe concentrations and subsequently treated with IL-1β. The production of inflammatory mediators including nitric oxide (NO), nitric oxide synthase (iNOS), as well as cyclooxygenase (COX)-2, and the expression of chondrogenic and hypertrophic markers including Sox 9, Aggrecan, Col 2a1, and matrix metalloproteinase-13 (MMP13) in the cells were measured. The effect of AA on nuclear factor-kappa B (NF-κB) signaling pathway was further determined by dual luciferase assay and western blot. The surgery-induced OA animals were treated with AA or saline for 6 weeks. The pathological changes in the affected joints were measured by micro-CT and histological analysis. Results: We found a broad safety spectrum of AA from 0 to 25 μM. A dose-dependent inhibitory effect of AA on NO production, as well as iNOS and COX-2 expression were found. Meanwhile, AA promoted chondrogenesis and inhibited hypertrophy in chondrocyte treated with IL-1β. In addition, AA inhibited NF-κB signaling pathway with a dose-dependent manner. Furthermore, results from animal study revealed that AA prevented articular cartilage damage as well as subchondral bone remodeling in the surgery-induced OA animal.

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“…It has many beneficial properties, including anti-inflammatory (16) and antioxidant (18) effects. Recently, AA has been demonstrated to control inflammation and exert protective effects via inhibiting NLRP3 inflammasome activation (16) and the NF-κB (19) pathway. However, the effects of AA on PID remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of Asiatic acid against pelvic inflammatory disease in rats

Kong

Fu²,

Zhang³

et al. 2019

Exp Ther Med

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Asiatic acid (AA) is one of the major components of the Chinese herb Centella asiatica and exerts a variety of pharmacological activities. However, the pharmacological effects of AA on pelvic inflammatory disease (PID) remain unknown. The purpose of the present study was to investigate the therapeutic efficacy and potential mechanisms of AA on PID in rats. A total of 75 female Sprague Dawley rats were randomly divided into the following five groups: A control group; a PID group; a PID + AA 5 mg/kg group; a PID + AA 35 mg/kg group; and a PID + AA 75 mg/kg group. Changes in cytokine and chemokine levels, myeloperoxidase (MPO) activity, nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome and nuclear factor-κB (NF-κB) activation, oxidative stress and cleaved caspase-3 were measured. AA treatment significantly decreased the excessive production of cytokines and chemokines and suppressed MPO activity and the activation of NLRP3 inflammasome, NF-κB and caspase-3, as well as oxidative stress. These results suggest that AA exhibits potent anti-inflammatory and antioxidant effects in rats with pathogen-induced PID and that the mechanism of these anti-inflammatory effects may be associated with the suppression of NLRP3 inflammasome activation and the NF-κB pathway.

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Asiatic acid inhibits pulmonary inflammation induced by cigarette smoke

Cited by 53 publications

References 93 publications

Asiatic Acid Exhibits Anti-inflammatory and Antioxidant Activities against Lipopolysaccharide and d-Galactosamine-Induced Fulminant Hepatic Failure

Asiatic Acid Exhibits Anti-inflammatory and Antioxidant Activities against Lipopolysaccharide and d-Galactosamine-Induced Fulminant Hepatic Failure

Asiatic Acid Attenuates Osteoarthritis by Regulating NF-κB Signaling Pathway in Chondrocytes

Protective effects of Asiatic acid against pelvic inflammatory disease in rats

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