三叉神经主要司职牙体和口颌面部的本体感觉传导,其膜表面有较高水平的瞬时受体电位香草酸亚型(TRPV)1表达。TRPV1属于瞬时受体电位离子通道家族成员之一,具有阳离子选择性,一经激活,可在三叉神经节和背根神经节介导疼痛及其传导。神经肽、缓激肽、前列腺素、神经生长因子和5-羟色胺等可以通过TRPV1通道直接刺激神经的疼痛感受器,引起疼痛敏感。温度和酸碱度亦可能引起相似的TRPV1通道结构改变。TRPV1的调控机制复杂并表现在诸多层面上,从基因转录、翻译和修饰到受体亚型的形成等,这些机制一方面维持TRPV1通道正常的生理功能,一方面也是造成其通道功能异常进而引起疼痛的根源。本文就TRPV1介导疼痛的机制和TRPV1的分子调控机制等研究进展作一综述。

Trigeminal nerve as mixed nerve mainly conducts the feeling coming from tooth and maxillofacial region. Transient receptor potential vanilloid(TRPV) 1 is highly expressed on the membrane of trigeminal ganglion. TRPV1 is one of the members of transient receptor potential(TRP) family, which is a kind of cation selective channel contributing to the conduction of pain based on trigeminal ganglion, dorsal root ganglion and so on. Nociception on nerve can be directly stimulated by neuropeptide, bradykinin, prostaglandin, nerve growth factor, 5-hydroxytryptamine, as well as temperature and pH, through TRPV1 as a result of pain. The regulatory mechanisms of TRPV1 are various and complex as on the processes like gene transcription, translation and expression as well as the formation of the receptor subtype. These mechanisms have effects on maintaining the normal physiological functions, also are the possible causes of dysfunction of TRPV1 leading to pain rising. In this review, the pain develop

目的在大鼠侧脑室内给予不同剂量的瞬时受体电位香草酸受体1(transient receptor potential vanilloid 1,TRPV1)拮抗剂Capsazepine,观察对LPS致热过程的影响。方法在侧脑室内预先给与3种剂量Capsazepine,随之腹腔给与LPS致热。在腹腔内埋植发射子遥测体温变化过程,同时应用荧光测定法检测下丘脑细胞内钙离子浓度的变化,Western blot方法检测TRPV1表达水平。结果随着Capsazepine剂量增大,LPS致大鼠发热水平升高,下丘脑细胞内钙离子浓度减少,TRPV1表达水平降低。结论 Capsazepine作用于大鼠下丘脑,可使LPS诱导的发热水平提高,此效应可能与TRPV1的作用有关。

Aim To observe the effects of the transient receptor potential vanilloid receptor 1 ( TRPV1 ) antago-nist Capsazepine on the LPS-induced fever process. Methods Three doses of Capsazepine were respec-tively injected into rats’ lateral ventricles before the in-traperitoneal injection of LPS caused fever. An emitter was implanted inside the rat’ s abdominal cavity to mo-nitor the body temperature changes during the fever process. Then the changes of calcium ion in the hypo-thalamus were detected by fluorescence and the expres-sions of TRPV1 protein were detected by Western blot.Results The higher dosage of Capsazepine was injec-ted, the higher the level of LPS-induced fever was, and the lower the concentration of calcium ion in the hypothalamus as well as the TRPV1 expressions were. Conclusion Capsazepine could increase the level of fever induced by LPS via acting on the rats’ hypothala-mus. This effect might be related to the functions of TRPV1 .

目的 探讨香草酸瞬时受体亚型1（transient receptor potential vanilloid 1,或vanilloid recepot 1,TRPV1）在电针调节胃运动中的作用.方法 选用TRPV1基因敲除小鼠（KO小鼠）及野生型C57BL/6小鼠（WT小鼠）,针刺足三里、曲池、中脘、胃俞穴,观察针刺前后胃内压变化.结果 电针WT小鼠足三里穴有兴奋,有抑制,表现为轻度兴奋为主.电针胃俞、曲池和中脘穴均表现为抑制效应.针刺KO小鼠足三里、曲池、中脘、胃俞穴,胃运动方向整体表现均为抑制.结论 TRPV1受体对胃运动有一定的调节作用,针刺TRPV1敲除小鼠可抑制胃运动.

ObjectiveTo discuss the role of transient receptor potential vanilloid 1 (TRPV 1) in the regulation effect of electroacupuncture on gastric motility.MethodTRPV1 gene knock-out mice (KO mice) and wild-type C57BL/6 mice (WT mice) were selected to receive acupuncture at Zusanli (ST36),Quchi (LI11), Zhongwan (CV12), and Weishu (BL21), and the intragastric pressure was observed before and after acupuncture.ResultElectroacupuncture at Zusanli caused both excitation and inhibition in WT mice, predominated by mild excitation, while electroacupuncture at Weishu, Quchi and Zhongwan all caused inhibition effect; in the KO mice, electroacupuncture at Zusanli, Quchi, Zhongwan, and Weishu all inhibited gastric motility.Conclusion TRPV1 bears certain regulating effect on gastric motility, andacupuncture can inhibit the gastric motility in TRPV gene KO mice.

目的：研究熊果酸（ursolic acid ，UA）对顺铂（cisplatin ，CDDP）致毒小鼠耳蜗瞬时感受器电位香草酸受体1（transient receptor potential vanilloid 1，TRPV1）表达的影响。方法60只健康BALB／c小鼠随机分成对照组（腹腔注射等量生理盐水）、UA组（腹腔注射熊果酸80 mg／kg）、CDDP组（腹腔注射CDDP 4．5 mg／kg）和CDDP＋UA组（一侧腹腔注CDDP 4．5 mg／kg ，同时对侧腹腔注射熊果酸80 mg／kg），每组15只。各组动物均连续腹腔注射给药5天，每天1次，给药前及停药后24 h行ABR检测，然后应用免疫组织化学染色、显微图像分析及蛋白质印迹技术观察小鼠耳蜗中TRPV1的表达。结果 CDDP组小鼠耳蜗TRPV1表达和ABR阈移均较对照组明显增加（P＜0．05），UA＋CDDP组小鼠ABR阈移及TRPV1表达较CDDP组明显降低（P＜0．05），且TRPV1表达变化与ABR阈移改变高度相关（｜r｜＞0．7，P＜0．05）。结论 UA可抑制CDDP所致TRPV1的高表达，有效降低CD_DP的耳毒性，改善听功能。

Objective To investigate the effects of ursolic acid (UA) on cisplatin (CDDP)-induced expres_sion of transient receptor potential vanilloid 1 (TRPV1) in mouse cochlea .Methods Sixty BALB/c mice were ran_domly divided into 4 groups (15 mice in each group) and received introperitoneal injection once daily for 5 days:Control group (normol saline) ,UA group (80 mg/kg/day) ,CDDP group (4 .5 mg/kg/day) ,and CDPP (4 .5 mg/kg/day) plus UA group (80 mg/kg/day) .The expression of TRPV1 in mouse cochlea was determined by immuno_histochemistry ,microscope image analysis and western blot ,and auditory thresholds were evaluated by auditory brainstem response (ABR) measurement .ResuIts The expression of cochlea TRPV1 and ABR threshold shift was significantly increased in the mice treated with CDDP (P 0 .7 , P<0 .05) .ConcIusion UA effectively attenuated CDDP -induced ototoxicity and improved auditory function through inhibition of TR_PV1 .

目的：探讨慢性非细菌性前列腺炎（chronic nonbacterial prostatitis，CNP）疼痛的可能机制。方法自身免疫法建立CNP大鼠模型；Von Frey丝检测机械刺激缩足阈（paw withdrawal threshold，PWT）；进行前列腺病理学检查和免疫组化检测前列腺与脊髓L5-S2节段c-fos、TRPV1的表达变化和相关性。结果造模后大鼠PWT下降，与对照组相比差异有统计学意义（P＜0.05）。前列腺呈现炎症反应，在病变范围、淋巴细胞浸润方面都较对照组显著，差异有统计学意义（P＜0.05）。与对照组相比，模型组前列腺与脊髓背角L5-S2中c-fos、TRPV1阳性表达均上调，差异有统计学意义（P＜0.05）。前列腺中与脊髓中的c-fos表达无相关关系（r =0.027，P =0.454）；并且两者的TRPV1表达也无相关关系（r =0.000，P=0.5）。结论 c-fos、TRPV1可能通过脊髓L5-S2节段的表达上调参与了CNP大鼠疼痛的形成和维持。

Objective To explore the possible mechanisms of chronic nonbacterial prostatitis pain. Methods The CNP rat model was established by the immune method. The pain threshold were detected by Von Frey filament. The expressions of c-fos and TRPV1 in the prostate and spinal L5- S2 segmental were detected by immunohistochemistry. Results The PWT of rat model group was significantly decreased as compared with that of the control group (P<0.05). There were significant inflammation in prostate tissues of rats. The differences in the scope of lesions and interstitial lymphocytic infiltrates were statistically significant between model group and the control group (P<0.05). The expressions of c-fos and TRPV1 in prostate and spinal cord dorsal horn L5 - S2 in model group were all upregulated remarkably compared with that of the control group (P<0.05). The expression of c-fos and TRPV1 in the prostate had no correlation with that in spinal cord (r =0.027,P =0.454; r = 0.000, P = 0.000). Conclusion For