Aqueous extract of Bruguiera gymnorrhiza leaves protects against dextran sulfate sodium induced ulcerative colitis in mice via suppressing NF-κB activation and modulating intestinal microbiota.

ETHNOPHARMACOLOGICAL RELEVANCE: Ulcerative colitis (UC) is tightly associated with inflammation response and oxidative stress. As a folk medicine applied in treatment of diarrhea, Bruguiera gymnorrhiza also possesses anti-inflammatory and anti-oxidative activities, which indicated that B. gymnorrhiza may exert anti-colitis effect. AIM OF THE STUDY: To investigate effect and mechanism of B. gymnorrhiza on experimental UC. MATERIALS AND METHODS: Aqueous extract of B. gymnorrhiza leaves (ABL) was used for investigation in the present study. Murine UC was established through access to 3% dextran sulfate sodium (DSS) for 7 days. Meanwhile, mice accepted treatment with ABL (25, 50, 100 mg/kg) or sulfasalazine (200 mg/kg) once daily. On the last day, disease activity index (DAI) including body weight loss, fecal character and degree of bloody diarrhea was evaluated, colon segments were obtained for length measurement and further analysis and feces were collected for intestinal microbiota analysis. RESULTS: ABL ameliorated DAI scores, colon length shortening and histopathological damage in DSS-induced colitis mice obviously. SOD activity, levels of MDA and GSH altered by colitis were restored remarkably after ABL treatment. ABL inhibited increases in levels of colonic COX-2, iNOS, TNF-α, IL-6, IL-1ß, IL-4, IL-10 and IL-11 in colitis mice. Moreover, ABL prominently suppressed NF-κB p65 and IκB phosphorylation and down-regulated mRNA levels of COX-2, iNOS, TNF-α, IL-6 and IL-1ß elevated by colitis. As shown in microbiota analysis, ABL modulated composition of intestinal microbiota of colitis mice. CONCLUSION: ABL exhibited protective effect against DSS-induced ulcerative colitis through suppressing NF-κB activation and modulating intestinal microbiota.

Origins of endomorphin-2 immunopositive fibers and terminals in the rat medullary dorsal horn.

Endomorphin-2-immunoreactive (EM2-IR) fibers and terminals are densely present in the medullary dorsal horn (MDH) and are key factors in regulating central nociceptive processing. However, the origins of these EM2-IR fibers and terminals remain elusive. It was hypothesized that there were at least three possible origins of the EM2-IR fibers and terminals in the MDH: intrinsic dorsal horn neurons, primary afferent fibers, and projection fibers from higher parts of the brain. Different kinds of measures were employed in the current study to elucidate this hypothesis. After intracerebral ventricle administration of colchicine, no EM2-IR neuronal cell bodies were detected in the MDH, suggesting that there was no intrinsic EM2-IR dorsal horn neuron. Disruption of bilateral primary afferents (exposed to the primary afferent neurotoxin, capsaicin) decreased bilateral EM2 expression but did not eliminate it. Transection of the trigeminal nerve sensory root significantly decreased EM2 expression on the ipsilateral but not on the contralateral MDH. After injecting FluoroGold (FG) into the MDH, FG retrogradely labeled some EM2-IR neurons in the bilateral hypothalamus and nucleus tractus solitarii (NTS), and some of the FG retrogradely labeled neurons in the ipsilateral trigeminal ganglion also showed EM2-immunoreactivities. These results indicate that EM2-IR fibers and terminals in the MDH come not only from ipsilateral primary trigeminal afferents but also from bilateral fibers from the hypothalamus and NTS.