Berberine modulates ASK1 signaling mediated through TLR4/TRAF2 via upregulation of miR-23a

Sujitha, Sali; Dinesh, Palani; Rasool, Mahaboobkhan

doi:10.1016/j.taap.2018.09.017

Cited by 23 publications

(12 citation statements)

References 48 publications

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“…TLR4 can anchor MyD88 and promote the nuclear translocation of NFκB to induce the expression of inflammatory factors [31]. In fact, some studies have found that the anti-inflammatory effect of BBR is related to TLR4 expression [32, 33]. In this study, macrophage inflammation and anti-inflammatory effects of BBR appeared after LPS intervention for 3 h and TLR4 protein levels did not increase at the same time.…”

Section: Discussionmentioning

confidence: 55%

Inhibitory effects of berberine on proinflammatory M1 macrophage polarization through interfering with the interaction between TLR4 and MyD88

Gong

Chen

et al. 2019

BMC Complement Altern Med

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BackgroundsInflammation is recognized as the key pathological mechanism of type 2 diabetes. The hypoglyceamic effects of berberine (BBR) are related to the inhibition of the inflammatory response, but the mechanism is not completely clear.MethodsThe inflammatory polarization of Raw264.7 cells and primary peritoneal macrophages were induced by LPS, and then effects and underlying mechanisms of BBR were explored. An inflammatory model was established by LPS treatment at different concentrations for different treatment time. An ELISA assay was used to detect the secretions of TNF-α. RT-PCR was applied to detect M1 inflammatory factors. The F4/80+ ratio and CD11c+ ratio of primary peritoneal macrophages were determined by flow cytometry. The expressions of p-AMPK and TLR4 were detected by Western blot. The cytoplasmic and nuclear distributions of NFκB p65 were observed by confocal microscopy. The binding of TLR4 to MyD88 was tested by CoIP, and the affinity of BBR for TLR4 was assessed by molecular docking.ResultsUpon exposure to LPS, the secretion of TNF-α and transcription of inflammatory factors in macrophages increased, cell morphology changed and protrusions appeared gradually, the proportion of F4/80+CD11c+ M1 macrophages increased, and the nuclear distribution of NFκB p65 increased. BBR pretreatment partially inhibited the changes mentioned above. However, the expression of TLR4 and p-AMPK did not change significantly after LPS intervention for 3 h. Meanwhile, CoIP showed that the interaction between TLR4 and MyD88 increased, and BBR inhibited the binding. Molecular docking suggested that BBR might interact with TLR4.ConclusionsInflammatory changes were induced in macrophages after LPS stimulation for 3 h, and BBR pretreatment inhibited inflammatory polarization. BBR might interact with TLR4 and disturb TLR4/MyD88/NFκB signalling pathway, and it might be the mechanism by which BBR attenuated inflammation in the early phase.

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Section: Discussionmentioning

confidence: 55%

Inhibitory effects of berberine on proinflammatory M1 macrophage polarization through interfering with the interaction between TLR4 and MyD88

Gong

Chen

et al. 2019

BMC Complement Altern Med

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“…BBR also inhibited the activation of the NLRP3 inflammasome pathway, and then improved liver injury in mice by inhibiting the purinoreceptor P2X7 92. TNFα and LPS stimulated the expression of miR-23a in RAW 264.7 macrophages, resulting in TLR4/TNF receptor-associated factor 2 (TRAF2)-mediated activation of apoptosis-signaling kinase 1 (ASK1) and phosphorylation of p38, which mediate inflammatory reaction 93. BBR treatment inhibited LPS and TNFα-induced inflammatory responses by up-regulating miR-23a, ameliorating TLR4, TRAF2, TNFα, IL-6 and IL-23 gene expression, and inhibiting TLR4/TRAF2-mediated ASK1/p38 phosphorylation 93.…”

Section: Bbr In the Treatment Of Cardiovascular Diseasesmentioning

confidence: 99%

“…TNFα and LPS stimulated the expression of miR-23a in RAW 264.7 macrophages, resulting in TLR4/TNF receptor-associated factor 2 (TRAF2)-mediated activation of apoptosis-signaling kinase 1 (ASK1) and phosphorylation of p38, which mediate inflammatory reaction 93. BBR treatment inhibited LPS and TNFα-induced inflammatory responses by up-regulating miR-23a, ameliorating TLR4, TRAF2, TNFα, IL-6 and IL-23 gene expression, and inhibiting TLR4/TRAF2-mediated ASK1/p38 phosphorylation 93. After percutaneous coronary intervention, macrophage activation plays an essential role in neovascular atherosclerosis and in-stent restenosis 94.…”

Section: Bbr In the Treatment Of Cardiovascular Diseasesmentioning

confidence: 99%

Berberine in Cardiovascular and Metabolic Diseases: From Mechanisms to Therapeutics

et al. 2019

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Cardiovascular and metabolic diseases (CVMD) are the leading causes of death worldwide, underscoring the urgent necessity to develop new pharmacotherapies. Berberine (BBR) is an eminent component of traditional Chinese and Ayurvedic medicine for more than 2000 years. Recently, BBR has attracted much interest for its pharmacological actions in treating and/or managing CVMD. Recent discoveries of basic, translational and clinical studies have identified many novel molecular targets of BBR (such as AMPK, SIRT1, LDLR, PCSK9, and PTP1B) and provided novel evidences supporting the promising therapeutic potential of BBR to combat CVMD. Thus, this review provides a timely overview of the pharmacological properties and therapeutic application of BBR in CVMD, and underlines recent pharmacological advances which validate BBR as a promising lead drug against CVMD.

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“…Subsequent isolation of primary synovial macrophages from the AIA rat treated with the p-coumaric acid-laden liposome showed impaired ability to perform osteoclastogenesis and bone resorption, compared to methotrexate-treated and untreated synovial macrophages [163]. In another follow-up study from the same group, Sujitha et al [164] incorporated berberine into the surface of the mannosylated liposome, which has been previously shown to induce silencing of inflammatory genes in macrophages through upregulation of microRNA (miRNA)-23a [165]. Using bone-marrow derived macrophages, the berberine-loaded mannosylated liposome demonstrated in vitro inhibition of osteoclastogenesis and impaired bone resorption ability in existing osteoclasts [164].…”

Section: Using Particles For Manipulation Of Ra-promoting Non-immune Cellsmentioning

confidence: 99%

Biomaterial-based immunotherapeutic strategies for rheumatoid arthritis

Lewis

2021

Drug Deliv. and Transl. Res.

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Berberine modulates ASK1 signaling mediated through TLR4/TRAF2 via upregulation of miR-23a

Cited by 23 publications

References 48 publications

Inhibitory effects of berberine on proinflammatory M1 macrophage polarization through interfering with the interaction between TLR4 and MyD88

Inhibitory effects of berberine on proinflammatory M1 macrophage polarization through interfering with the interaction between TLR4 and MyD88

Berberine in Cardiovascular and Metabolic Diseases: From Mechanisms to Therapeutics

Biomaterial-based immunotherapeutic strategies for rheumatoid arthritis

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