Liang-Ge-San, a classic traditional Chinese medicine formula, protects against lipopolysaccharide-induced inflammation through cholinergic anti-inflammatory pathway

Liu, Junshan; Wei, Xiduan; Lu, Zibin; Xie, Pei; Zhou, Huixia; Chen, Yuyao; Ma, Jia-Mei; Yu, Linzhong

doi:10.18632/oncotarget.8452

Cited by 15 publications

(13 citation statements)

References 38 publications

(45 reference statements)

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“…However, these pro-inflammatory cytokines were significantly inhibited after LGS treatment. Moreover, LGS at the concentration of 200 µg/ml showed the similar anti-inflammatory activity compared with that of dexamethasone (DEX) (100 µM) ( Figures 1B and S2 ), which was consistent with our previous research (Liu et al, 2016). We also investigated the cytotoxicity and the anti-inflammatory activity of marker compounds of LGS in RAW264.7 cells.…”

Section: Resultssupporting

confidence: 91%

“…Clinical observation found that LGS, a famous traditional Chinese medicine formula, could inhibit ALI (Wang et al, 2011; Lee et al, 2017). In previous studies, we demonstrated that LGS significantly suppressed LPS-stimulated ALI by activating the cholinergic anti-inflammatory pathway (Liu et al, 2016), but also inhibited the protein expression of STAT3 in lung tissue of ALI rats (Liu et al, 2009).…”

Section: Discussionmentioning

confidence: 96%

“…Generally, adult patients take orally 200 ml of LGS decoction at the dosage of 0.195 g/ml twice per day according to the suggestion of traditional Chinese medicine. In previous studies, we have revealed that LGS suppresses ALI by activating the cholinergic anti-inflammatory pathway, which leads to the inhibition of the NF-κB pathway (Liu et al, 2016). Based on our previous research, whether other modulators are associated with anti-inflammatory effects of LGS needs further explored.…”

Section: Introductionmentioning

confidence: 99%

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Liang-Ge-San, a Classic Traditional Chinese Medicine Formula, Attenuates Lipopolysaccharide-Induced Acute Lung Injury Through Up-Regulating miR-21

Yang

Huo

et al. 2019

Front. Pharmacol.

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Background: Acute lung injury (ALI) is a life-threatening disease without effective chemotherapy at present. Liang-Ge-San (LGS) is a famous traditional Chinese medicine formula, which is used to treat ALI in China. However, only a few studies have addressed the mechanisms of LGS in ALI. Purpose: To evaluate the anti-inflammatory effects of LGS on lipopolysaccharide (LPS)-induced ALI, and to explore its underlying molecular mechanism. Methods: Murine RAW264.7 cells were treated with LGS and LPS (1 μg/ml). The generation of IL-6, TNF-α, IL-1β was detected by ELISA. The protein expressions of STAT3 and P-STAT3 (Tyr705) were determined by Western blotting and fluorescence confocal microscopy. STAT3 transcriptional activity was investigated by luciferase reporter gene assay. qPCR was used to detect the expressions of microRNA-21 (miR-21), STAT3, and IL-6. DSS cross-linking assay was used to assess the change of STAT3 dimer. In vivo anti-inflammatory effects of LGS were evaluated in an ALI mouse model induced by tracheal instillation of LPS (3 mg/kg). The anti-ALI effects were evaluated by ELISA, qPCR, Western blotting, BCA, and H&E assays. Results: LGS suppressed LPS-stimulated IL-6, TNF-α, and IL-1β generation in murine macrophages RAW264.7. Moreover, LGS down-regulated protein levels of P-STAT3 (Tyr705) and STAT3, inhibited STAT3 transcriptional activity, and up-regulated miR-21. Furthermore, blockage of miR-21 antagonized the inhibitory effects of LGS on the production of IL-6 and the expressions of P-STAT3 (Tyr705) and STAT3 as well as the formation of STAT3 dimer. Critically, LGS up-regulated the expression of miR-21 and inhibited the protein expressions of STAT3 and P-STAT3 (Tyr705) to reduce the release of IL-6 and inflammatory cell infiltration as well as the degree of edema in LPS-induced ALI mice. Conclusion: LGS inhibited LPS-induced ALI through up-regulating miR-21 and subsequently inhibiting the STAT3 signaling pathway, thereby decreasing the release of IL-6.

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Section: Resultssupporting

confidence: 91%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

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Liang-Ge-San, a Classic Traditional Chinese Medicine Formula, Attenuates Lipopolysaccharide-Induced Acute Lung Injury Through Up-Regulating miR-21

Yang

Huo

et al. 2019

Front. Pharmacol.

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“…Cells or rodents are traditionally used to study and screen antiendotoxic drugs [40-42]. However, drugs that have antiendotoxic effects in vitro may be ineffective in vivo .…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Phillyrin on Lethal LPS-Induced Neutrophil Inflammation in Zebrafish

Lei

Zhou

Huang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Forsythia suspensa Vahl. (Oleaceae) fruits are widely used in traditional Chinese medicine to treat pneumonia, typhoid, dysentery, ulcers and oedema. Antibacterial and anti-inflammatory activities have been reported for phillyrin (PHN), the main ingredient in Forsythia suspensa Vahl fruits, in vitro. However, the underlying mechanisms in vivo remain poorly defined. In this study, we discovered that PHN exerted potent anti-inflammatory effects in lethal LPS-induced neutrophil inflammation by suppressing the MyD88-dependent signalling pathway in zebrafish. Methods: LPS-yolk microinjection was used to induce a lethal LPS-infected zebrafish model. The effect of PHN on the survival of zebrafish challenged with lethal LPS was evaluated using survival analysis. The effect of PHN on neutrophil inflammation grading in vivo was assessed by tracking neutrophils with a transgenic line. The effects of PHN on neutrophil production and migration were analysed by SB⁺ cell counts during consecutive hours after modelling. Additionally, key cytokines and members of the MyD88 signalling pathway that are involved in inflammatory response were detected using quantitative RT-PCR. To assess gene expression changes during consecutive hours after modelling, the IL-1β, IL-6, TNF-α, MyD88, TRIF, ERK1/2, JNK, IκBa and NF-κB expression levels were measured. Results: PHN could protect zebrafish against a lethal LPS challenge in a dose-dependent manner, as indicated by decreased neutrophil infltration, reduced tissue necrosis and increased survival rates. Up-regulated IL-1β, IL-6 and TNF-α expression also showed the same tendencies of depression by PHN. Critically, PHN significantly inhibited the LPS-induced activation of MyD88, IκBa, and NF-κB but did not affect the expression of ERK1/2 MAPKs or JNK MAPKs in LPS-stimulated zebrafish. Additionally, PHN regulated the MyD88/IκBα/NF-κB signalling pathway by controlling IκBα, IL-1β, IL-6, and TNF-α expression. Conclusion: This study provides a rationale for the clinical application of PHN as an anti-inflammatory agent.

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“…Traditional Chinese medicines (TCMs) have shown efficacy in the management of many inflammatory diseases[ 4 ]. The most famous formula for the treatment of SAP is Qingyi decoction, which is composed of rheum, Chinese thorowax root, white peony root, baikal skullcap root, coptis chinensis, and other herbs and has been advocated for more than one hundred years in China[ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells

Zhou

Bie

et al. 2018

WJG

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AIMTo investigate the effects of combined use of emodin and baicalein (CEB) at the cellular and organism levels in severe acute pancreatitis (SAP) and explore the underlying mechanism.METHODSSAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD rats. Pancreatic histopathology score, serum amylase activity, and levels of tumour necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and IL-10 were determined to assess the effects of CEB at 12 h after the surgery. The rat pancreatic acinar cells were isolated from healthy male SD rats using collagenase. The cell viability, cell ultrastructure, intracellular free Ca2+ concentration, and inositol (1,4,5)-trisphosphate receptor (IP3R) expression were investigated to assess the mechanism of CEB.RESULTSPancreatic histopathology score (2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05) and serum amylase activity (2866.2 ± 617.7 vs 5241.3 ± 1410.0, P < 0.05) were significantly decreased in the CEB (three doses) treatment group compared with the SAP group (2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05). CEB dose-dependently reduced the levels of the pro-inflammatory cytokines IL-6 (466.82 ± 48.55 vs 603.50 ± 75.53, P < 0.05) and TNF-α (108.04 ± 16.10 vs 215.56 ± 74.67, P < 0.05) and increased the level of the anti-inflammatory cytokine IL-10 (200.96 ± 50.76 vs 54.18 ± 6.07, P < 0.05) compared with those in the SAP group. CEB increased cell viability, inhibited cytosolic Ca2+ concentration, and significantly ameliorated intracellular vacuoles and IP3 mRNA expression compared with those in the SAP group (P < 0.05). There was a trend towards decreased IP3R protein in the CEB treatment group; however, it did not reach statistical significance (P > 0.05).CONCLUSIONThese results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that CEB is a suitable approach for SAP treatment.

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Liang-Ge-San, a classic traditional Chinese medicine formula, protects against lipopolysaccharide-induced inflammation through cholinergic anti-inflammatory pathway

Cited by 15 publications

References 38 publications

Liang-Ge-San, a Classic Traditional Chinese Medicine Formula, Attenuates Lipopolysaccharide-Induced Acute Lung Injury Through Up-Regulating miR-21

Liang-Ge-San, a Classic Traditional Chinese Medicine Formula, Attenuates Lipopolysaccharide-Induced Acute Lung Injury Through Up-Regulating miR-21

Protective Effect of Phillyrin on Lethal LPS-Induced Neutrophil Inflammation in Zebrafish

Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells

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