| Background:Pain is one of the most serious symptoms which affect the life quality of patients with endometriosis. So far the mechanism is still not clearly defined. Recent research has found out that the patients with endometriosis has different distribution in small sensory C-and Aδfibers, and there is obvious relationship between the pain and the increase of small sensory-C and Aδfibers. Our previous study has proved the distribution of nerve fibers in different endometriosis tissues and the relationship with pain. However, it is hard to explain the difference in duration and depth of pain only with the increase of fibers. In 2004, people knew the increase of sodium channel expression was a import reason of pain through primary erythermalgia. Ion channels which trigger pain is tightly relative to the occurrence of pain. Beside that, this paper will try to describe the possible reason of endometriosis associated pain from the ion channel point of view. Transient receptor potential vanilloid subtype-1 (TRPV1) is the most known member of TRP super family. TRPV1 can be activated by diverse range of chemical ligands such as capsaicin and other vanilloids, as well as acid (protons, H+, PH<5.9), physical stimuli such as heat (> 43℃), certain arachidonic acid derivatives and direct phosphorylation via protein kinase C. After activation, TRPV1 can reinforce the sensibility of pain sense in sensory nerve endings and affect the pain duration. Ten years after the cloning of TRPV1,com pel ling data has been gathered on the role of this channel in inflammatory and neuropathic states, even in some unknown reason painful disease(irritable bowel syndrome, painful bladder syndrome, etc). As we known, there is still no research about the relationship between TRPV1 and the pain triggered by endometriosis.Objective:1. To investigate the difference between the expression of TRPV1 in sacro ligament with endometriosis and its correlation with pain.2. To determine whether TRPV1 in the functional layer endometrium were caused by endometriosis itself or a common symptom of pain.3. To explore the expression of TRPV1 in ectopic implants and CNS.Method:1. Specimens(endometrium and ectopic lesion) were immunostained using specific antibodies to TRPV1. Western Blot and Real time PCR were performed to detect TRPV1 in endometriosis lesions and eutopic endometrium.2. After rat model of endometriosis was built, we observed TRPV1'expression in focies had been increased.3. By rat model of chronic dysmenorrhea, we understood there was an "obviously differents of dysmenorrhea between endometriosis group and the control one. And after painful stimulating, there was a statistical different in the central nervous system.Result:1. In endometriosis sacral ligament, moderate to severe painful group's TRPV1 expression was significantly higher than the light or no pain group. It is very close relation to TRPV1's expression and pain.2. In the same degree of painful patients, endometriosis had more TRPV1 than other none endometriosis group.3. The sensitivity of the endometriosis group was significantly higher than control's in function layer of endometrium. But the differences and the extent of pain had no relationship.4. Endometriosis played a important role in TRPV1'promotion. Mounting evidence now suggested that TRPV1 receptors on the central branches of dorsal root ganglion neurons in the spinal cord might play an important role in modulation of pain and nociceptive transmission.Conclusion:1. TRPV1 is in the presence of glandular epithelium with endometriosis. In endometriosis(sacro-ligaments), the painful degree is obviously correlated with TRPV1's expression.2. Functional layer of the endometrial glandular epithelial expression of TRPV1 is not the pain of endometriosis arising from the difference. The ectopic endometrium and specific micro-environment maybe interact the results.3. Animal experiments prove that endometriosis is one of the reasons which could upregulate the TRPV1's expression. |
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