Evodiamine has therapeutic efficacy in ulcerative colitis by increasing Lactobacillus acidophilus levels and acetate production

Wang, Meng-Xia; Li, Lin; Chen, Yong-Da; Zhong, Yuanyuan; Lin, Yixuan; Li, Pei; Tian, Xing; Han, Bo; Xie, Zenghong; Liao, Qiongfeng

doi:10.1016/j.phrs.2020.104978

Cited by 91 publications

(51 citation statements)

References 72 publications

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“…The present study demonstrated for the first time, to the best of the authors' knowledge that Evo could effectively reduce LPS-induced NPCs apoptosis, ECM degradation and inflammation, possibly by upregulating SIRT1 and activating the PI3K/Akt pathway. evo, as an effective ingredient of Traditional chinese medicine, has a variety of pharmacological effects such as antioxidant, anti-tumor, anti-ulcer and neuroprotection, especially in anti-infection and anti-apoptosis (10,11). Evo, for example, inhibits p2x7-dependent TnF-α expression and ERK1/2 phosphorylation, thereby inhibiting oxidative stress and inflammatory response (28).…”

Section: Discussionmentioning

confidence: 99%

“…Evodiamine (Evo), a type of indole quinazoline alkaloid extracted from dried fruit of Evodia rutaecarpa (8). in traditional chinese medicine, Evodia rutaecarpa is widely used for treating various infection-related diseases, such as diarrhea, ulcerative colitis and beriberi (9)(10)(11), showing strong anti-inflammatory activity. A previous study suggested that Evo can enhance NLRP3 inflammasome activation by inducing α-tubulin acetylation, thereby improving innate immunity to bacterial infections (11).…”

Section: Introductionmentioning

confidence: 99%

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Upregulation of SIRT1 by Evodiamine activates PI3K/AKT pathway and blocks intervertebral disc degeneration

Kuai¹,

Zhang

2022

Mol Med Rep

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intervertebral disc degeneration (idd) is a major cause of a number of spinal diseases, resulting in serious public health problems. evodiamine (evo) is an indole quinazoline alkaloid extracted from Evodia rutaecarpa, which has antioxidant, anti-apoptosis and anti-inflammatory effects. The purpose of the present study was to investigate lipopolysaccharide (LPS)-induced IDD progression in human nucleus pulposus cells (nPcs) and its potential mechanism. The viability and apoptosis of NPCs were detected by Cell Counting Kit-8 (CCK-8) and TUNEL staining, respectively. Western blotting was used to detect the expression levels of proteins, cell transfection was performed to knockdown Sirtuin 1 (SirT1) and the expression of tumor necrosis factor-alpha (TnF-α) and interleukin 6 (il-6) was detected by enzyme-linked immunosorbent assay kits. The results showed that Evo effectively alleviated LPS-induced NPCs apoptosis and caspase-3 activation and evo treatment reversed the upregulation of matrix metalloproteinase-13, as well as the downregulation of collagen type II (collagen II), Sry-type high-mobility-group box 9 and aggrecan and reduced the production of pro-inflammatory factors TNF-α and il-6 in lPS-stimulated nPcs. in addition, treatment with evo upregulated SirT1 and activated the Pi3K/Akt pathway, knockdown of SIRT1 inhibited the phosphorylation of Akt and PI3K in lPS-stimulated nPcs. in general, evo upregulated SirT1 and inhibited lPS-induced nPcs apoptosis, extracellular matrix degradation and inflammation by activating the PI3K/akt pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Upregulation of SIRT1 by Evodiamine activates PI3K/AKT pathway and blocks intervertebral disc degeneration

Kuai¹,

Zhang

2022

Mol Med Rep

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“…L. acidophilus can also inhibit endoplasmic reticulum stress (ER), thereby alleviating intestinal inflammation (14). In addition, evodiamine can relieve dextran sulfate sodium (DSS)-induced colitis by increasing L. acidophilus in the intestine (15). Selenium (Se) is an important trace element in the human body that has antioxidant and anti-inflammatory effects and has an important influence on human immunity (16,17).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Selenium-Enriched Lactobacillus acidophilus Ameliorates Dextran Sulfate Sodium-Induced Chronic Colitis in Mice by Regulating Inflammatory Cytokines and Intestinal Microbiota

Pan

Jiang

et al. 2021

Front. Med.

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Aim: To evaluate the effect of Selenium-enriched Lactobacillus acidophilus (Se-enriched L. acidophilus) on dextran sulfate sodium (DSS)-induced colitis in mice.Methods: Mice were randomly divided into four groups: a control group, a control + Se-enriched L. acidophilus group, a chronic colitis group, and a chronic colitis + Se-enriched L. acidophilus group (n = 10 each group). The mice were sacrificed on the 26th day. The disease activity index, survival rates, and histological injury score were determined. Cytokines produced by lamina propria lymphocytes (LPLs), the selenium (Se) concentrations in serum and colon tissue and the mouse intestinal microbiota were evaluated.Results: Se-enriched L. acidophilus can improve histological injury and the disease activity index in mice with chronic colitis and reduce IL-1β, IL-6, IL-12p70, TNF-α, IL-23, IFN-γ, IL-17A, and IL-21 (P < 0.05) and increase IL-10 (P < 0.05) expression levels. Moreover, Se-enriched L. acidophilus can increase the β diversity of intestinal microbiota in mice with chronic colitis, significantly reduce the relative abundance of Lactobacillus and Romboutsia (P < 0.05), and significantly increase the relative abundance of Parasutterella (P < 0.05).Conclusions: Se-enriched L. acidophilus can improve DSS-induced chronic colitis by regulating inflammatory cytokines and intestinal microbiota.

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“…[9][10][11][12][13] Moreover, our previous research has confirmed that the effect of evodiamine on UC was highly related to the increased abundance of L. acidophilus in the intestine, and then it was proved that the active form of L. acidophilus can repair the intestinal barrier damage caused by UC. 14 Additionally, SCFAs, as the host-gut microbiota metabolites, are responsible for mediating the interactions between gut microbiota and the host. 15 Evidence shows that SCFAs promote intestinal homeostasis by inhibiting histone deacetylase (HDAC) activity or activating G proteincoupled receptors (GPRs) on the intestinal cell surface.…”

Section: Introductionmentioning

confidence: 99%

Live Lactobacillus acidophilus alleviates ulcerative colitis via the SCFAs/mitophagy/NLRP3 inflammasome axis

Chen

Zhang

et al. 2022

Food Funct.

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Evodiamine has therapeutic efficacy in ulcerative colitis by increasing Lactobacillus acidophilus levels and acetate production

Cited by 91 publications

References 72 publications

Upregulation of SIRT1 by Evodiamine activates PI3K/AKT pathway and blocks intervertebral disc degeneration

Upregulation of SIRT1 by Evodiamine activates PI3K/AKT pathway and blocks intervertebral disc degeneration

Selenium-Enriched Lactobacillus acidophilus Ameliorates Dextran Sulfate Sodium-Induced Chronic Colitis in Mice by Regulating Inflammatory Cytokines and Intestinal Microbiota

Live Lactobacillus acidophilus alleviates ulcerative colitis via the SCFAs/mitophagy/NLRP3 inflammasome axis

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