ABSTRACT
Aim To investigate the effect of chlorogenic acid (CGA) on chronic inflammatory pain induced by complete Freund's adjuvant (CFA) and to observe the influence of CGA on CFA-induced synaptic expression of AMAP receptor in spinal dorsal horn. Methods CFA was injected intraplantarly into the hindpaws of mice to induce mechanical allodynia and thermal hyperalgesia. The changes of paw withdrawal threshold (PWT) and the paw withdrawal latency (PWL) were tested after intrathecal administration of CGA. Meanwhile, the synaptic expression and phosphorylation of AMPA receptor subunit were assessed by immunoblot-ting. Results The intrathecal injection of CGA produced dose-depended improvement of both PWT and PWL in CFA injected mice. A higher dose of CGA (200ng) did not influence the base thresholds of normal mice. The median dose of CGA (100 ng) effectively reversed the CFA-induced synaptic expression of GluAl; meanwhile, it suppressed the phosphorylation of GluAl at Ser845, with no influence on phosphorylation at Ser831. Conclusions CGA might exert its analgesic effect by specifically inhibiting the phosphorylation of GluAl -Ser845 and the synaptic incorporation of GluAl-containing AMPA receptor.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of berberine on the release of nitric oxide (NO) by rat intestinal mucous microvascular endothelial cells (RIMECs) cultured in vitro for exploring the pharmacological mechanism of berberine in treating intestinal disease.</p><p><b>METHODS</b>Cultured RIMECs in vitro were identified adopting immunofluorescent stain with factor VIII-related antigen. NO level in the supernatant of normal cell culture or cell culture treated with different concentrations of berberine was detected with colorimetry at the 3rd, 6th, 9th and 12th h and compared.</p><p><b>RESULTS</b>Compared with that in the normal control group, NO level increased more obviously in the berberine treated groups, and the best effect was shown in the 5 microg/mL berberine treated group.</p><p><b>CONCLUSION</b>One of the important pharmacological mechanisms of berberine might be through promoting the endogenous NO release to induce endothelium-dependent dilatation of microvascular in intestinal mucosa, thus to improve the local microcirculation of intestine.</p>