Therapeutic effect of a hydroxynaphthoquinone fraction on dextran sulfate sodium-induced ulcerative colitis

Fan, Hui; Yang, Mingyan; Zhang, Zuo-Kai; Liu, Ke

doi:10.3748/wjg.v20.i41.15310

Cited by 27 publications

(20 citation statements)

References 33 publications

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“…Overall disease severity was assessed by a clinical scoring system, and a disease activity index (DAI) score was calculated for each animal (Zhang et al, 2014). …”

Section: Methodsmentioning

confidence: 99%

Fecal Microbiota Transplantation Ameliorates Experimentally Induced Colitis in Mice by Upregulating AhR

et al. 2018

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Ulcerative colitis (UC) is a chronic non-specific inflammatory disease that occurs in the colon and rectum. While fecal microbiota transplantation (FMT) is gaining attention as a clinical treatment of UC, the molecular mechanisms behind this effect have yet to be fully understood. A C57BL/6 mouse model was established to test whether FMT promotes the recovery of colon inflammation. Administration of 2% dextran sulfate sodium (DSS) for 7 days successfully induced acute colitis, as evidenced by diarrhea, hematochezia and colon shortening as well as a decrease in body weight. FMT alleviated the severity of colon mucosa injury and improved histological alterations compared with that of the DSS group. In addition, FMT promoted homeostasis of the intestinal microbiota. Furthermore, FMT upregulated the expression of aryl hydrocarbon receptor (AHR), interleukin-10 (IL-10), and transforming growth factor beta (TGF-β) in colon tissues. These results suggest that the significant anti-inflammatory effect of FMT may be attributed to its promotion of IL-10 and TGF-β production and AHR activation. Based on these results, FMT had a favorable therapeutic effect on DSS-induced colitis.

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“…Overall disease severity was assessed by a clinical scoring system, and a disease activity index (DAI) score was calculated for each animal (Zhang et al, 2014). …”

Section: Methodsmentioning

confidence: 99%

Fecal Microbiota Transplantation Ameliorates Experimentally Induced Colitis in Mice by Upregulating AhR

et al. 2018

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“…In the present study, the levels of TNF-α and IL-1β were markedly upregulated during the onset of DSS-induced colitis induction. Treatment of ulcerative colitis commonly reduces inflammatory cell infiltration and the levels of serum TNF-α and IL-1β (31,32). In particular, treatment with TNF-α neutralizing antibody or TNF-α inhibitory agents significantly improveds colitis (33,34).…”

Section: Discussionmentioning

confidence: 99%

Ursolic acid protects against ulcerative colitis via anti-inflammatory and antioxidant effects in mice

Liu

Piao

Guo

et al. 2016

Molecular Medicine Reports

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Abstract. Ursolic acid (UA) has been reported to have a protective effect in colitis. However, the underlying mechanisms remain to be elucidated. In the present study, experimental ulcerative colitis was induced in male BALB/c mice by the administration of 5% dextran sulfate sodium (DSS) for 7 days, followed by treatment with UA for another 7 days. Hematoxylin & eosin staining was performed to evaluate colon tissue damage, and enzyme assays were used to measure malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in colon homogenate. In addition, serum levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α were measured using an ELISA, and the level of nuclear factor (NF)-κB p65 in the colonic tissues was assessed by western blotting. The 7-day DSS administration induced marked colon damage, increased the serum levels of IL-1β and TNF-α, increased MDA content and decreased SOD activity in the colon homogenate. These changes were significantly improved by treatment with UA. UA also reduced the DSS-stimulated high nuclear level of NF-κB p65 in the colon tissues. These results demonstrate a protective role of UA in ulcerative colitis, and suggest that anti-inflammatory and antioxidant activities are involved in the underlying mechanisms.

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“…The symptoms in mice with DSS-induced UC are very similar to those of human UC, suggesting that it is an ideal model for study. These symptoms include disruption to the epithelial cell barrier, colitis induced by altered DNA replication, inhibition of the growth of epithelial cells, induction of macrophage activation, increased release of cytokines and disruption to the balance of gut microflora (5). The disease has become a target of research into new therapies, due to the fact it causes recurrent attacks, has a poor therapeutic response, leads to prolonged illness and has the possibility of developing into cancer (6,7).…”

Section: Introductionmentioning

confidence: 99%

Intrarectally administered polaprezinc attenuates the development of dextran sodium sulfate‑induced ulcerative colitis in mice

Xie

Liu

et al. 2019

Exp Ther Med

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/kg). After the animals were sacrificed, blood was collected and the serum levels of NF-κB and tumor necrosis factor-α (TNF-α) were measured. Changes in histology were observed by light microscopy. The protein levels of AKT, phosphorylated AKT and heat shock protein 70 (HSP70) were determined by western blot analysis. The results suggested that PZ reduced the DSS-induced increase in the inflammatory proteins TNF-α and NF-κB in the UC model. The high-dose of PZ also increased the HSP70 protein level, inhibited AKT phosphorylation in a DSS-induced UC animal model, and decreased white blood cell and neutrophil % counts compared to levels in an untreated DSS control group. Histopathology indicated that the mice of the DSS model group had irregular colonic villi, a large number of inflammatory cells and mucosal damage, whereas mice of the group treated with PZ had small intestinal villus morphology and their villi showed signs of recovery from the damage of UC. The results of the present study indicated that PZ significantly alleviates DSS-induced UC in mice, relieves diarrhea, and inhibits the phosphorylation of inflammatory factors and the inflammatory AKT signaling pathway.

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Therapeutic effect of a hydroxynaphthoquinone fraction on dextran sulfate sodium-induced ulcerative colitis

Abstract: HM had a favorable therapeutic effect on DSS-induced ulcerative colitis, supporting its further development and clinical application in inflammatory bowel disease.

Cited by 27 publications

References 33 publications

Fecal Microbiota Transplantation Ameliorates Experimentally Induced Colitis in Mice by Upregulating AhR

Fecal Microbiota Transplantation Ameliorates Experimentally Induced Colitis in Mice by Upregulating AhR

Ursolic acid protects against ulcerative colitis via anti-inflammatory and antioxidant effects in mice

Intrarectally administered polaprezinc attenuates the development of dextran sodium sulfate‑induced ulcerative colitis in mice

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