Triptolide attenuates LPS-induced activation of RAW 264.7 macrophages by inducing M1-to-M2 repolarization via the mTOR/STAT3 signaling

Zhu, Huanhuan; Tong, Shaopeng; Yan, Congrong; Zhou, A-Cheng; Wang, Minying; Li, Chunwei

doi:10.1080/08923973.2022.2093738

Cited by 12 publications

(3 citation statements)

References 33 publications

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“…M2 macrophages, induced by IL-4, IL-10, IL-13 contribute to tissue healing and fibrosis [58]. In experimental and human IBD, M1 prevails over M2 macrophages, and molecules able to invert this trend, such as baicalin, IL-33, lactic acid bacteria or plant derived flavonoids, allow for the reduction of the severity of intestinal inflammation promoting mucosal healing, partly through the activation of Wnt signaling [64][65][66][67][68][69][70][71][72].…”

Section: Dendritic Cells and Macrophagesmentioning

confidence: 99%

Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases

Padoan

Musso

Contran

et al. 2023

CIMB

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In this review, the role of innate and adaptive immunity in the pathogenesis of inflammatory bowel diseases (IBD) is reported. In IBD, an altered innate immunity is often found, with increased Th17 and decreased Treg cells infiltrating the intestinal mucosa. An associated increase in inflammatory cytokines, such as IL-1 and TNF-α, and a decrease in anti-inflammatory cytokines, such as IL-10, concur in favoring the persistent inflammation of the gut mucosa. Autoinflammation is highlighted with insights in the role of inflammasomes, which activation by exogenous or endogenous triggers might be favored by mutations of NOD and NLRP proteins. Autoimmunity mechanisms also take place in IBD pathogenesis and in this context of a persistent immune stimulation by bacterial antigens and antigens derived from intestinal cells degradation, the adaptive immune response takes place and results in antibodies and autoantibodies production, a frequent finding in these diseases. Inflammation, autoinflammation and autoimmunity concur in altering the mucus layer and enhancing intestinal permeability, which sustains the vicious cycle of further mucosal inflammation.

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Section: Dendritic Cells and Macrophagesmentioning

confidence: 99%

Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases

Padoan

Musso

Contran

et al. 2023

CIMB

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“…We investigated the anti-in ammatory effects of CUR. LPS administration could induce the expression of proin ammatory cytokines such as IL-6, IL-1β and TNF-α (Bhatia et al, 2022, Zhu et al, 2022. To further verify CUR has anti-in ammatory effects, we measured the level of IL-6, IL-1β and TNF-α in serum by ELISA.…”

Section: Cur Reduced Lps-induced In Ammatory Response Through Pi3k-ak...mentioning

confidence: 99%

Mechanistic insights into the anti-depressant effect of curcumin based on network pharmacology and experimental validation

Guo

Fang

Xiong

et al. 2023

Preprint

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Growing evidence supports the involvement of neuroinflammation in the pathophysiology of depression. Administrating curcumin could revert the depressive-like symptoms and weakened microglial activation and increased the level of pro-inflammatory cytokine. This study aimed to identify potential anti-depression targets and mechanisms of curcumin (CUR) by an approach of network pharmacology. GSEA and KEGG pathways showed the most significantly enriched pathway of CUR against depression was the PI3K-Akt pathway. Moreover, 52 targets were significantly correlated with PI3K-Akt signaling pathway and CUR-related targets. In addition, among these top 50 targets which were ranked by degree in the PPI network, there were 23 targets involved in the 52 intersection targets. Thus, our findings suggest that CUR exerts its anti-depression effects through PI3K-Akt signaling pathway. Furthermore, we investigated the anti-depression effects of CUR using a mouse model of depression induced by lipopolysaccharide (LPS). Administration of LPS alone (2 mg/kg/day, i.p.) extended the immobility time in the open filed test (OFT) and tail suspension test (TST), decreased sucrose consumption in the sucrose preference test (SPT). Pretreatment with CUR (50 mg/kg/day, i.p.) for 7 consecutive days relieved LPS-induced changes in the behavior tests, the activity of PI3K-Akt signaling pathway, neuronal damage in the PFC and inflammatory response. Moreover, inhibition of the PI3K-Akt signaling pathway by LY294002 (7.5 mg/kg/day, i.p.) blocks the therapeutic effects of CUR. In conclusion, our study indicate that CUR may be an effective antidepressant agent for LPS-induced mouse model, in part because of its anti-inflammatory actin through PI3K-Akt signaling pathway.

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“…Triptolide (TP), a bioactive epoxy-2-terpenoid ester compound isolated from the traditional Chinese medicine Tripterygium wilfordii Hook F., has been used for treating various diseases for over a hundred years [ 6 , 7 ]. Its beneficial physiological properties have been demonstrated in different areas, such as anti-tumor [ 8 , 9 ], anti-inflammatory [ 10 , 11 ], and immunomodulatory [ 12 ] effects.…”

Section: Introductionmentioning

confidence: 99%