Deoxyschizandrin suppresses dss-induced ulcerative colitis in mice

Zhang, Wenfeng; Yang, Yan; Su, Xin; Xu, Da-yan; Yan, Yunqi; Gao, Qun; Duan, Minghua

doi:10.4103/1319-3767.195552

Cited by 10 publications

(7 citation statements)

References 39 publications

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“…The present study explored the effects of YMJ on DSS-induced mouse models of UC. The DSS-induced UC mouse model is a common experimental method used to investigate intestinal inflammation ( 31 ). Previous studies have shown that YMJ can improve mucosal injury, and can reduce the extent and severity of injury ( 22 , 32 ).…”

Section: Discussionmentioning

confidence: 99%

Leonurine protects against ulcerative colitis by alleviating inflammation and modulating intestinal microflora in mouse models

et al. 2021

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Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the colon. The aim of the present study was to explore the effects of leonurine (YMJ) on inflammation and intestinal microflora in colonic tissues of a dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mouse model. Mice were randomly divided into control (n=5), DSS (n=5, treated with DSS) and DSS+YMJ (n=5, treated with DSS and YMJ) groups. Body weight was recorded, disease activity index (DAI) was calculated, and colon histopathology was evaluated using hematoxylin and eosin staining. Serum interleukin (IL)-6, tumor necrosis factor-α (TNF-α) and IL-1β levels were examined using ELISA. Expression levels of nuclear factor-κB (p65) and phosphorylated (p)-p65 were evaluated via western blotting. 16S ribosomal RNA was extracted from mouse feces. Composition or abundance changes of intestinal microflora were analyzed. The results indicated that YMJ treatment (DSS+YMJ group) significantly increased body weight, reduced DAI scores and increased colon length in UC mouse models compared with those in the DSS group (P<0.05). YMJ significantly reduced inflammatory infiltration, significantly decreased serum TNF-α, IL-6 and IL-1β levels (P<0.05) and significantly downregulated the p-p65/p65 ratio compared with the DSS group (P<0.05). YMJ increased the quantity of the intestinal flora and improved intestinal microflora diversity in the mice of the DSS group. Specifically, YMJ partly regulated intestinal microflora in feces, including a reduction of Bifidobacterium , and an increase in Parasutterella and Ackermania . In conclusion, YMJ improved disease outcomes of the UC mice, reduced the levels of serum inflammatory factors and increased the ratio of beneficial bacteria in the intestinal tract.

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Section: Discussionmentioning

confidence: 99%

Leonurine protects against ulcerative colitis by alleviating inflammation and modulating intestinal microflora in mouse models

et al. 2021

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“…The mice were randomly divided into 7 groups, 10 in each group: control group (CON group), UC model group (UC group), sulfasalazine positive control group (SASP group), chlorogenic acid low dose group (CGA-L group), chlorogenic acid middle dose group (CGA-M group), chlorogenic acid high dose group (CGA-H group), and ERK inhibitor plus chlorogenic acid treatment group (E+CGA group). In addition to the CON group, the ulcerative colitis model was made as described in the literature [25]. The dextran sodium sulfate (DSS) was dissolved in distilled water to prepare a 5% DSS solution, and the mice were allowed to freely drink the solution for 7 days, and then to drink distilled water for 14 days.…”

Section: Methodsmentioning

confidence: 99%

Chlorogenic Acid Attenuates Dextran Sodium Sulfate-Induced Ulcerative Colitis in Mice through MAPK/ERK/JNK Pathway

Gao

Wang

et al. 2019

BioMed Research International

148

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Objective. Observe the protective effect of chlorogenic acid on dextran sulfate-induced ulcerative colitis in mice and explore the regulation of MAPK/ERK/JNK signaling pathway. Methods. Seventy C57BL/6 mice (half males and half females) were randomly divided into 7 groups, 10 in each group: control group (CON group), UC model group (UC group), and sulfasalazine-positive control group (SASP group), chlorogenic acid low dose group (CGA-L group), chlorogenic acid medium dose group (CGA-M group), chlorogenic acid high dose group (CGA-H group), and ERK inhibitor + chlorogenic acid group (E+CGA group). The effects of chlorogenic acid on UC were evaluated by colon mucosa damage index (CMDI), HE staining, immunohistochemistry, ELISA, and Western blot. The relationship between chlorogenic acid and MAPK/ERK/JNK signaling pathway was explored by adding ERK inhibitor. Results. The UC models were established successfully by drinking DSS water. Chlorogenic acid reduces DSS-induced colonic mucosal damage, inhibits DSS-induced inflammation, oxidative stress, and apoptosis in colon, and reduces ERK1/2, p -ERK, p38, p-p38, JNK, and p-JNK protein expression. ERK inhibitor U0126 reversed the protective effect of chlorogenic acid on colon tissue. Conclusion. Chlorogenic acid can alleviate DSS-induced ulcerative colitis in mice, which can significantly reduce tissue inflammation and apoptosis, and its mechanism is related to the MAPK/ERK/JNK signaling pathway.

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“…BDNF possesses significant effects on differentiation, growth, and damage restoring and could maintain the normal function of sensory nerve [16, 17]. The increased level of BDNF may result in various abnormal feelings related to pains such as chronic pain, inflammatory pain, visceral pain, and high sensitivity [18].…”

Section: Introductionmentioning

confidence: 99%

Effects of Deoxyschisandrin on Visceral Sensitivity of Mice with Inflammatory Bowel Disease

Zhang

Dou

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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The aims of this study were to build an IBD mouse model and further to observe the effects of deoxyschisandrin on IBD and visceral sensitivity and to evaluate the relevance of brain-derived neurotrophic factor (BDNF) to intestinal hypersensitivity of IBD mice. The results showed that deoxyschisandrin could depress the contraction of isolated smooth muscle, modulate gastrointestinal function, and efficiently decrease the disease activity index (DAI) of IBD mice, which proved that deoxyschisandrin had antidiarrheal effects on the animals. In the colorectal distention (CRD) experiment, visceral sensibility was increased in the model group. However, abdominal withdrawal reflex (AWR) scores were decreased after deoxyschisandrin intervention, indicating that deoxyschisandrin could reduce the visceral hypersensitivity of IBD mice. Both IHC observation and western blotting analysis showed that BDNF protein expression increased evidently in colon of IBD mice. After the intervention of deoxyschisandrin, colon mucosa BDNF protein expression in IBD mice decreased, indicating that deoxyschisandrin could decrease mouse intestinal sensitivity by reducing colon mucosa BDNF expression. In conclusion, deoxyschisandrin possessed antidiarrheal effects and visceral hypersensitivity inhibitory effects in the mice with IBD induced by TNBS, which was related to the reduction in BDNF expression in the colon.

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Deoxyschizandrin suppresses dss-induced ulcerative colitis in mice

Cited by 10 publications

References 39 publications

Leonurine protects against ulcerative colitis by alleviating inflammation and modulating intestinal microflora in mouse models

Leonurine protects against ulcerative colitis by alleviating inflammation and modulating intestinal microflora in mouse models

Chlorogenic Acid Attenuates Dextran Sodium Sulfate-Induced Ulcerative Colitis in Mice through MAPK/ERK/JNK Pathway

Effects of Deoxyschisandrin on Visceral Sensitivity of Mice with Inflammatory Bowel Disease

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