To study the preventive effect of
sophocarpine (Soc) on
dextran sulfate sodium (DSS)-induced
colitis in mice, in order to analyze the influence of Soc on
toll like receptor 4 (TLR4)/
mitogen-activated protein kinases (MAPKs) and janus
tyrosine kinase 2 signal transducer and activator of transcription 3 (JAK2/STAT3) signal pathways in mice intestinal tissues. The mice was given 2.5% DSS for 6 days to induce the acute
colitis model. The Soc-treated group was intraperitoneally injected with
sophocarpine 30 mg · kg(-1) · d(-1) since the day before the experiment to the end. The disease activity index (DAI) was assessed everyday, and the colonic morphology and histological damage were observed with HE staining. The
mRNA expressions of
tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and
interleukin-6 (IL-6) were detected by real-time RT-PCR. The changes in key
protein kinase p38 mitogen-activated protein kinase (p38MAPK), c-Jun NH2-terminal
protein kinase1/2 (JNK1/2), extracellular signal-regulated kinase1/2 (ERK1/2), JAK2, STAT3 in TLR4/MAPKs and JAK2/STAT3 signaling pathways were detected by western blot. The result showed that the model group showed statistical significance in
body weight, DAI, colon length and histopathological changes compared with the normal group (P <0.05); however, the Soc-treated group showed significant improvements in the above indexes compared with the model group (P <0.05). TNF-α, IL-1β and
IL-6 in the model group was significantly higher than that in the normal group (P <0.05), but lowered in the Soc-treated group to varying degrees (P <0.05). In the normal group, the expressions of TLR4 and the phosphorylation of P38, JNK1/2, JAK2, STAT3 were at low levels; in the model group, the phosphorylation of P38, JNK1/2, JAK2, STAT3 increased; the Soc-treated group showed a decrease in TLR4 expression compared with the model group, with notable declines in the phosphorylation of TLR4, P38, JNK1/2, JAK2, STAT3. These findings indicate that Soc can inhibit TLR4/MAPKs, K2/STAT3 signaling pathway activation, reduce the expression of proinflammatory
cytokines TNF-α, IL-1β and
IL-6 and relieve inflammatory reactions, so as to effectively prevent experimental
colitis.