Published online Dec 21, 2017. doi: 10.3748/wjg.v23.i47.8308
Peer-review started: September 7, 2017
First decision: October 10, 2017
Revised: November 3, 2017
Accepted: November 14, 2017
Article in press: November 14, 2017
Published online: December 21, 2017
Processing time: 105 Days and 0.5 Hours
Panax notoginseng (PN) is a Chinese herbal medicine commonly used to treat ulcerative colitis (UC) and vascular diseases. Microvascular injury plays an important role in the pathogenesis of UC, but PN’s effects on microvascular injury in UC are unclear. To clarify the effects of PN on microvascular injury is important for treating UC.
The effects of PN on microvascular injury in colitis, its initial administration time, its dosage and its related mechanisms were investigated. These are important questions for using PN for treatment of UC.
To clarify the effects of PN on microvascular injury and related affecting factors, as well as its mechanisms.
Dextran sodium sulfate (DSS)- or iodoacetamide (IA)-induced rat colitis models were used. PN administration was initiated at 3 d and 7 d after the model was established at doses of 0.5, 1.0 and 2.0 g/kg for seven consecutive days. The severity of colitis was evaluated by disease activity index (DAI). The pathological lesions were observed under microscope. Microvessel density (MVD) was evaluated by immunohistochemistry. Vascular permeability was evaluated using the Evans blue method. The serum concentrations of vascular endothelial growth factor (VEGF)A121, VEGFA165, interleukin (IL)-4, IL-6, IL-10 and tumor necrosis factor (TNF)-α were detected by enzyme-linked immunosorbent assay. Myeloperoxidase (MPO) and superoxide dismutase (SOD) were measured to evaluate the level of oxidative stress. Expression of hypoxia-inducible factor (HIF)-1α protein was detected by western blotting. One-way ANOVA or general linear model with repeated measures was used to analyze the data sets with three or more groups, and least significant difference post hoc test for multiple comparisons. Student’s t-test was used to analyze data sets with two groups. P < 0.05 was considered significant.
Obvious colonic inflammation and injuries of colonic mucosa and microvessels were observed in DSS- and IA-induced colitis in rats. DAI scores, the serum concentrations of VEGFA121, VEGFA165, VEGFA165/VEGFA121, IL-6 and TNF-α, and the concentrations of MPO and HIF-1α in the colon were significantly higher while the serum concentrations of IL-4 and IL-10 and MVD in colon were significantly lower in the colitis model groups than in the normal control group. PN promoted repair of the injuries of colonic mucosa and microvessels, attenuated inflammation and decreased DAI scores in rats with colitis. PN decreased the serum concentrations of VEGFA121, VEGFA165, VEGFA165/VEGFA121, IL-6 and TNF-α and the concentrations of MPO and HIF-1α in the colon. It also increased the serum concentrations of IL-4 and IL-10 as well as the concentration of SOD in the colon. The efficacy of PN was dosage dependent. In addition, DAI scores in the group initiating PN administration on day 3 were significantly lower than in the group initiating PN administration on day 7.
PN repaired microvessel injury in experimental colitis via attenuating inflammation and oxidative stress in the colonic mucosa. The efficacy of PN was related to the initial administration time and the dose.
Finding the real effective component in PN and clarifying the mechanisms of PN attenuating oxidative stress and regulating angiogenesis will be conducted in the future studies.