Effects of initiating time and dosage of Panax notoginseng on mucosal microvascular injury in experimental colitis

Figure 1 Efficacy of Panax notoginseng in experimental colitis was dependent on initial time of administration. A: PN administration (1.0 g/kg) was initiated at day 3 and 7 for seven consecutive days; B, C, G, J: DAI scores and serum concentrations of TNF-α and IL-6 in the day 3 group were significantly lower than those in the day 7 group; D, E: The pathological lesions of colonic mucosa and microvessels in the day 3 group were less than those in the day 7 group; F: MVD in the day 3 group was significantly higher than that in the day 7 group. Results are expressed as mean ± SD of three independent experiments performed in triplicate. ^aP < 0.05, ^bP < 0.01 vs normal control. DAI: Disease activity index; IL: Interleukin; MVD: Microvessel density; PN: Panax notoginseng; TNF: Tumor necrosis factor.

Figure 2 Panax notoginseng improved hypoxia in colonic mucosa. A-F: Increased expression of hypoxia-inducible factor-1α in colonic mucosa of the experimental colitis group was down-regulated by PN in a time- and dose-dependent manner. Results are expressed as mean ± SD of three independent experiments performed in triplicate. ^aP < 0.05, ^bP < 0.01 vs normal control. PN: Panax notoginseng.

Figure 3 Panax notoginseng blocked oxidative stress in colonic mucosa. Activities of MPO and SOD in colonic tissue were used to evaluate the anti-oxidative effect of PN. A-D: The increased activity of MPO and decreased activity of SOD in the experimental colitis groups were reversed by PN in a time- and dose-dependent manner. Results are expressed as mean ± SD of three independent experiments performed in triplicate. ^aP < 0.05, ^bP < 0.01 vs normal control. MPO: Myeloperoxidase; PN: Panax notoginseng; SOD: Superoxide dismutase.

Figure 4 Panax notoginseng repaired colonic mucosal injuries and microvessels. IA- and DSS-induced experimental colitis groups were treated with PN (0.5, 1.0 and 2.0 g/kg) for seven consecutive days. A, C: Colonic mucosal injuries and microvessels significantly improved; B, D, E: Microvessel density increased compared with the control groups in a dose-dependent manner. Results are expressed as mean ± SD of three independent experiments performed in triplicate. ^bP < 0.01 vs normal control. DSS: Dextran sodium sulfate; IA: Iodoacetamide; PN: Panax notoginseng.

Figure 5 Panax notoginseng improved impaired vascular permeability. A and B: Increased VP in the IA- and DSS-induced experimental colitis groups was decreased by medium and high doses of PN. Results are expressed as mean ± SD of three independent experiments performed in triplicate. ^bP < 0.01 vs normal control. DSS: Dextran sodium sulfate; IA: Iodoacetamide; PN: Panax notoginseng; VP: Vascular permeability.

Figure 6 Panax notoginseng reversed the disordered ratio of VEGFA165/VEGFA121 and adjusted the imbalance of pro-inflammatory and anti-inflammatory cytokines. A-C: Increased serum concentrations of VEGF165 and VEGF121, as well as the increased ratio of VEGF165/VEGF121 in the experimental colitis groups were down-regulated by medium and high doses of PN; D-F: The increased serum concentrations of IL-6 and TNF-α and decreased serum concentrations of IL-4 and IL-10 in the experimental colitis groups were reversed by PN in a dose-dependent manner. Results are expressed as mean ± SD of three independent experiments performed in triplicate. ^aP < 0.05, ^bP < 0.01 vs normal control. IL: Interleukin; PN: Panax notoginseng; TNF: Tumor necrosis factor; VEGF: Vascular endothelial growth factor.