A polyphenolic flavonoid glabridin: Oxidative stress response in multidrug-resistant Staphylococcus aureus

Singh, Vigyasa; Pal, Anirban; Darokar, Mahendra P.

doi:10.1016/j.freeradbiomed.2015.06.016

Cited by 79 publications

(52 citation statements)

References 59 publications

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“…The pathological changes of the lung tissue in the LPS+GLA groups were less severe than that in the LPS alone groups, suggesting that glabridin yields anti-oxidation activity both in brain and lung tissue. This study confirmed that glabridin could alleviate LPS-induced lung injury in rats through its strong antioxidant effects, which is consistent with previous studies [6]. NO is more than an inflammatory mediator.…”

Section: Discussionsupporting

confidence: 93%

“…Only several drugs are proven to be effective in the treatment of lung injury. Glabridin, a traditional Chinese herbal, is the main ingredient of licorice flavonoids with broad biological activity: antioxidant [4], anti-inflammatory [5], regulation of energy metabolism, antibacterial [6] and skin whitening, etc. In murine macrophages and microglia, licorice flavonoids have been shown to inhibit the release of prostaglandin E2 (PGE2), IL-1, nitric oxide (NO) and TNF-α.…”

Section: Discussionmentioning

confidence: 99%

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Glabridin attenuates lipopolysaccharide-induced acute lung injury by inhibiting p38MAPK/ERK signaling pathway

et al. 2016

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BackgroundAcute respiratory distress syndrome (ARDS) is a complication caused by pulmonary and/or external factors. In this study, we investigated the protective mechanisms of glabridin in lipopolysaccharide (LPS) induced ARDS in rats.ResultsGLA treatment at dose of 30 mg/kg decreased LPS-induced lung W/D ratio and alleviated evident lung histopathological changes. Expressions of TNF-α and IL-18 were suppressed by GLA in plasma. The levels of SPA, MDA and NO in lung were down-regulated significantly in groups administrated with GLA. While the SOD level increased after GLA administration. Additionally, the attenuation of inflammatory responses by GLA was closely associated with p38MAPK/ERK pathway, and the expressions of protein p-p38MAPK and pERK were inhibited by GLA in LPS-induced ARDS rats.Materials and MethodsSixty-four Wistar rats were randomly assigned into control group, Glabridin (GLA) alone group, LPS groups (6 h, 12 h, 24 h), GLA with LPS groups (6 h, 12 h, 24 h). ARDS was induced in rats by intraperitoneal administration of LPS (10 mg/kg). The degree of lung edema was evaluated by calculating the wet/dry weight ratio. The levels of inflammatory mediators, tumor necrosis factor-α (TNF-α) and interleukin-18 (IL-18) were assayed by enzyme-linked immunosorbent assay (ELISA). Surfactant protein A (SPA), malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) were analyzed. Pathological changes of lung tissues were observed by H&E staining. The protein expression of p38MAPK and ERK was detected using immunohistochemical techniques. Lung phosphorylated p38MAPK (p-p38MAPK) and pERK protein expression changes were detected by Western blotting.ConclusionsGlabridin significantly ameliorated the lung injury induced by LPS in rats via the inhibition of p38MAPK and ERK signaling pathway, antioxidant effect and reducing inflammation.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Glabridin attenuates lipopolysaccharide-induced acute lung injury by inhibiting p38MAPK/ERK signaling pathway

et al. 2016

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“…A cluster of proteins involved in oxidative stress responses was found to be up-regulated in response to the UA-norfloxacin combination in MRSA-2071 cells, which is in accordance with the earlier report where similar results were obtained in MRSA cells exposed to sub-inhibitory concentrations of UA [44]. Oxidants such as ROS and NO affect the viability of cells and hinder the process of pathogenesis [56] by irreversible oxidative damage to DNA, lipids and proteins [57,58] and bring the tissues to homeostasis [59,60]. The treatment further decreased the expression of some of the proteins involved in peptidoglycan and fatty acid biosynthesis.…”

Section: Alteration Of Membrane Permeability and Potentialsupporting

confidence: 91%

Usnic acid modifies MRSA drug resistance through down‐regulation of proteins involved in peptidoglycan and fatty acid biosynthesis

et al. 2019

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Multidrug‐resistant Staphylococcus aureus infections place a huge burden on the healthcare sector and the wider community. An increasing rate of infections caused by methicillin‐resistant Staphylococcus aureus (MRSA) has necessitated the development of alternative agents. We previously reported that usnic acid (UA) has activity against MRSA; here, we report the effect of UA in combination with norfloxacin on the drug resistance of MRSA clinical isolates. We observed that the combination of UA–norfloxacin significantly reduces the bacterial burden in mouse models infected with S. aureus, without causing any detectable associated toxicity. Proteomic analysis indicated that UA–norfloxacin induces oxidative stress within cells, which leads to membrane damage and inhibits metabolic activity and biosynthesis of peptidoglycan and fatty acids. Collectively, this study provides evidence that UA in combination with norfloxacin may be a potential candidate for development into a resistance‐modifying agent for the treatment of invasive MRSA infections.

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“…Glabridin, a polyphenolic flavonoid extracted from a traditional medicine, Glycyrrhiza glabra (licorice) root, was first isolated and characterized in 1976 . Glabridin has been associated with numerous biological properties; it has antioxidant, anti‐inflammatory, antiatherosclerotic, cardiovascular protective, energy metabolism regulating, immunomodulatory, estrogenic, neuroprotective, antiosteoporotic, antinephritic, antibacterial, antifungal, antiobesity, radical scavenging, and skin‐whitening activities . Studies have indicated that glabridin has antitumor effects, including antiproliferation effects in liver and breast cancers; antimetastatic effects in liver, breast, and lung cancers; antiangiogenetic effects in breast and lung cancers; inhibitory effects on the cancer stem cell–like properties in breast and lung cancers; and antiapoptotic effects in leukemia and liver cancers.…”

Section: Introductionmentioning

confidence: 99%

Glabridin induces apoptosis and cell cycle arrest in oral cancer cells through the JNK1/2 signaling pathway

Chen

Hsieh

et al. 2018

Environmental Toxicology

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Glabridin, a flavonoid extracted from licorice (Glycyrrhiza glabra), possesses various biological properties, including anticancer activities. However, the effect of glabridin on oral cancer cell apoptosis and the underlying molecular mechanisms has not been elucidated. In this study, we demonstrated that glabridin treatment significantly inhibits cell proliferation in human oral cancer SCC-9 and SAS cell lines. Flow cytometric assays demonstrated that glabridin induced several features of apoptosis, such as sub-G1 phase cell increase and phosphatidylserine externalization. Furthermore, glabridin induced apoptosis dose-dependently in SCC-9 cells through caspase-3, -8, and -9 activation and poly (ADP-ribose) polymerase cleavage. Moreover, glabridin increased the phosphorylation of the extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase (JNK) pathways in a dose-dependent manner. Moreover, the inhibition of the JNK1/2 inhibitor significantly reversed the glabridin-induced activation of the caspase pathway. In conclusion, our findings suggest that glabridin induces oral cancer cell apoptosis through the JNK1/2 pathway and is a potential therapeutic agent for oral cancer.

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A polyphenolic flavonoid glabridin: Oxidative stress response in multidrug-resistant Staphylococcus aureus

Cited by 79 publications

References 59 publications

Glabridin attenuates lipopolysaccharide-induced acute lung injury by inhibiting p38MAPK/ERK signaling pathway

Glabridin attenuates lipopolysaccharide-induced acute lung injury by inhibiting p38MAPK/ERK signaling pathway

Usnic acid modifies MRSA drug resistance through down‐regulation of proteins involved in peptidoglycan and fatty acid biosynthesis

Glabridin induces apoptosis and cell cycle arrest in oral cancer cells through the JNK1/2 signaling pathway

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