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鞘内注射MK-801在福尔马林诱导的大鼠炎性疼痛过程中抑制海马的一氧化氮合酶(NOS)活性和一氧化氮(NO)含量。

[Intrathecal injection of MK-801 inhibited the NOS activity and NO content of hippocampus in rat during the process of formalin-induced inflammatory pain].

作者信息

Liu Ling-yun, Li Qing-jun, Hu Yu-yan, Guo Xin-hua, Chu Sai-chun, Li Wen-bin

机构信息

Department of Pathophysiology, Basic Medical college, Hebei Medical University, Shijiazhuang 050017, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2009 Aug;25(3):423-7.

PMID:21155253
Abstract

AIM

To study the effect of intrathecal injection of MK-801, a NMDA receptor antagonist, on the NOS activity and NO content of hippocampus in rat during the process of formalin-induced inflammatory pain as well as the pain behavior of rat.

METHODS

The degree of pain was determined by observing the time of licking and biting the injected paw. NOS expression in the hippocampus was determined by using NADPH-d histochemical staining. NO content of hippocampus was determined by assaying NO3; and NO2.

RESULTS

Subcutaneous injection of formalin elicited a characteristic pain behavioural response consisting of licking and biting the injected paw, etc. Intrathecal injection of MK-801 could shorten obviously the time of licking and biting representing pain behavioural response in phase 2. It is suggested that intrathecal injection of MK-801 could block the pain behavioural response induced by formalin (P < 0.05). The number and staining degree of NADPH-d positive neurons in formalin group significantly increased at 12 h after the formalin injection in CA1, CA2-3 and DG of hippocampus compared with control group as well as NO content, however, the number and staining degree of NADPH-d positive neurons in formalin + MK-801 group significantly decreased in contrast to those of formalin 12 h group as well as the NO content (P < 0.01).

CONCLUSION

Intrathecal injection of NMDA receptor antagonist MK-801 could inhibit the NOS activity and NO production in hippocampus of rat, which showed the increase of hippocampal NO production was mainly induced by the peripheral nociceptive information input.

摘要

目的

研究鞘内注射N-甲基-D-天冬氨酸(NMDA)受体拮抗剂MK-801对福尔马林诱导的炎性疼痛大鼠海马中一氧化氮合酶(NOS)活性、一氧化氮(NO)含量以及大鼠疼痛行为的影响。

方法

通过观察舔咬注射足的时间来确定疼痛程度。采用还原型辅酶Ⅱ-黄递酶(NADPH-d)组织化学染色法测定海马中NOS的表达。通过检测NO3⁻和NO2⁻来测定海马中NO的含量。

结果

皮下注射福尔马林引发了包括舔咬注射足等特征性疼痛行为反应。鞘内注射MK-801可明显缩短代表第二相疼痛行为反应的舔咬时间。提示鞘内注射MK-801可阻断福尔马林诱导的疼痛行为反应(P<0.05)。与对照组相比,福尔马林注射后12小时,福尔马林组海马CA1、CA2-3和齿状回(DG)中NADPH-d阳性神经元的数量和染色程度显著增加,NO含量也增加;然而,与福尔马林12小时组相比,福尔马林+MK-801组中NADPH-d阳性神经元的数量和染色程度以及NO含量均显著降低(P<0.01)。

结论

鞘内注射NMDA受体拮抗剂MK-801可抑制大鼠海马中NOS的活性和NO的产生,表明海马中NO产生的增加主要是由外周伤害性信息输入诱导的。

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Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2009 Aug;25(3):423-7.
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