[Effect of triptolide on iNOS and SP expressions in spinal dorsal horn and dorsal root ganglion of rats with adjuvant arthritis].

OBJECTIVE: To observe the analgesic effect of triptolide (TP) of high, middle and low doses on rats with adjuvant arthritis (AA), and the expressions of inducible nitric oxide synthase (iNOS) and substance P (SP) in spinal dorsal horn and dorsal root ganglion (DRG) of corresponding sections, in order to discuss the possible mechanism for the analgesic effect of TP on rats with adjuvant arthritis. METHOD: Fifty SD rats were selected and randomly divided into the normal group (group A), the model group (group B), and TP low (group C), middle (group D), high (group E) dose groups. Except for the group A, all of the remaining groups were injected with 0.1 mL of Freund's complete adjuvant through their right rear toes to establish the model. At 14 d after the model establishment, rats in C, D and E groups were intraperitoneally injected with different doses of TP (0.1 mg x kg(-1) for the group C, 0.2 mg x kg(-1) for the group D, 0.4 mg x kg(-1) for the group E) once a day for 9 days. Then the 50% mechanical withdraw threshold (MWT) was determined. And the expressions of iNOS and SP in lumbar5 (L5) spinal dorsal horn and DRG were detected with the immunohistochemical method. RESULT: The 50% MWT of rats in the group B was significantly lower than that of the group A (P < 0.01). After being treated with TP, the Thermal withdrawal latencies of groups C, D and E were significantly higher than that of the group B (P < 0.01). TP could notably increase the MWT of AA rats, with a certain dose-effect relationship. The immunohistochemical results indicated that the iNOS and SP expressions significantly increased in the group B (P < 0.01), while the positive expression levels of iNOS and SP in groups C, D and E were significantly lower than that of the group B (P < 0.01), with a certain dose-effect relationship. CONCLUSION: TP shows a good analgesic effect on AA, and could inhibit the iNOS and SP expressions in spinal dorsal horn and DRG in rats with adjuvant arthritis, which may be one of action mechanisms for the analgesic effect of TP.

[Effect of Triptolide on expression of NMDAR1 and BSI-B4 binding sites in spinal dorsal horn and dorsal root ganglion in rats with adjuvant arthritis].

OBJECTIVE: To study the analgesic effect of Triptolide(TP) in rats with adjuvant and the possible mechanism. METHODS: Fifty healthy SD rats were randomly divided into normal control group (group A), model group (group B), and low(group C), middle (group D) and high(group E) dose TP treatment groups. Except the group A, each group of rats were reared by toe intradermal injection of 0. 1 mL Freund's complete adjuvant. After 14 days,rats in the C, D and E groups were taken different doses (0. 1 mg/kg group C, 0. 2mg/kg group D, and 0. 4 mg/kg group E) by intraperitoneal injection of TP for 9 days, and then thermal withdrawal latency and the expression of NMDAR1 and BSI-B4 binding sites in lumbar5 (L5) spinal dorsal horn and DRG were detected. RESULTS: Thermal withdrawal latency of rats in group B was significantly lower than that of group A (P <0. 01), while those in group C, D and E were significantly higher than those in group B (P <0. 05 or P <0. 01). TP increased the thermal pain threshold by a quantity-effect relationship; NMDAR-1 and BSI-B4 binding sites expression levels were significantly increased in group B than those in group A (P <0. 01), while those in group C, D and E were lower than those in group B. CONCLUSION: Analgesic effect of TP is related to reducing levels of expression of NMDAR1 and BSI-B4 binding sites in spinal dorsal horn and DRG in rats with adjuvant arthritis.

[Influence of triptolide on neuronal apoptosis in rat with cerebral injury after focal ischemia reperfusion].

OBJECTIVE: To study effect of triptolide (TL) on neuronal apoptosis in cerebral tissue of rat after ischemia-reperfusion. METHOD: Triptolide at dose 0.2 or 0.4 mg x kg(-1) was intraperitoneally injected once a day for 4 d. The focal cerebral ischemia-reperfusion model was established with thread embolism in middle artery before triptolide injection on the fourth day. Neurological deficit score of rats was evaluated; and immunohistochemical techniques were used to count positive cells of express of MPO and TUNEL in cerebraltissue. RESULT: Compared with the control group, the deficit of neural function was significantly improved, and the number of infiltrate of neutrophil and neuronal apoptosis in cerebral tissue was remarkably reduced in two TL-treated groups. CONCLUSION: The results suggested that TL can inhibit infiltration of neutrophil and decrease the degree of neuronal apoptosis in cerebral tissue.