| DC 欄位 |
值 |
語言 |
| DC.contributor | 生命科學系 | zh_TW |
| DC.creator | 黃真 | zh_TW |
| DC.creator | Jen Wong | en_US |
| dc.date.accessioned | 2017-10-6T07:39:07Z | |
| dc.date.available | 2017-10-6T07:39:07Z | |
| dc.date.issued | 2017 | |
| dc.identifier.uri | http://ir.lib.ncu.edu.tw:88/thesis/view_etd.asp?URN=103821014 | |
| dc.contributor.department | 生命科學系 | zh_TW |
| DC.description | 國立中央大學 | zh_TW |
| DC.description | National Central University | en_US |
| dc.description.abstract | 長期發炎性疼痛主要是發炎反應產生時會釋放發炎相關介質，其會活化或調控傷害感受器，導致疼痛和痛覺敏感的現象產生。發炎介質中的酸會造成組織酸化，其為引發疼痛的重要因素。有二類酸敏性受體，一是酸敏感性離子通道，另一個則是酸敏感性G蛋白耦合受體。酸敏感性G蛋白耦合受體，包含OGR1、 GPR4、 G2A和TDAG8，可以表現在小直徑的痛覺神經中。TDAG8在注射CFA後1天表現量會增加，而G2A則是在90分鐘時增多。將TDAG8基因表現量降低可以延遲CFA所誘導的痛覺敏感現象，而過度表現G2A則可以降低CFA所引起的早期的痛覺敏感現象。這些研究指出TDAG8可能有促進疼痛的角色，而G2A則是有抑制疼痛的角色。然而，目前其它酸敏感性G蛋白耦合受體在發炎性疼痛中所扮演的角色仍然不清楚。為了解決這個問題，我的實驗中使用short-hairpin RNA (shRNA)來抑制酸敏感性G蛋白耦合受體的基因，探討他們在疼痛上的角色。我發現抑制OGR1會在CFA注射後4小時減緩機械性痛覺敏感現象，並且減少粒細胞的數量。而抑制G2A除延長機械性痛覺敏感現象外，另會在42天增加粒細胞的數量。抑制GPR4雖會延長痛覺敏感現象，但並不會改變免疫細胞數量的變化。 | zh_TW |
| dc.description.abstract | Chronic inflammatory pain results from inflammation that releases the mediators to activate or modulate the nociceptors, leading to pain and hyperalgesia. Tissue acidosis appears to be a dominant factor in inflammatory pain, and the acidosis signals can be sensed by the proton-sensing ion channels and G proton-coupled receptors (GPCRs). The proton-sensing GPCRs, Ovarian cancer G protein-coupled receptor 1 (OGR1), G protein-coupled receptor 4 (GPR4), G2 accumulation (G2A), and T-cell death associated gene 8 (TDAG8), were found in small-diameter nociceptors, and TDAG8 expression was increased at 1 day, while G2A expression increased at 90 minutes after CFA inflammation. The inhibition of TDAG8 delays the onset of CFA-induced hyperalgesia, whereas overexpression of G2A reduced hyperalgesia at the early phase. These results suggested that TDAG8 may have a pro-nociceptive role, and G2A have an anti-nociceptive role in CFA-induced hyperalgesia. However, the roles of other proton-sensing GPCRs in inflammatory pain are still unclear. To address this issue, proton-sensing GPCRs were knocked down with short hairpin RNA. I have found that OGR1 knockdown mice significantly reduced mechanical hyperalgesia and decreased the number of granulocytes at 4 hours after CFA injection. Moreover, knockdown of G2A prolonged mechanical hyperalgesia and increased the number of granulocytes at 42 days, whereas GPR4 knockdown mice prolonged hyperalgesia but did not change the number of immune cells. | en_US |
| DC.subject | 酸敏感性G蛋白耦合受體 | zh_TW |
| DC.subject | 完全弗氏佐劑 | zh_TW |
| DC.subject | OGR1 | en_US |
| DC.subject | G2A | en_US |
| DC.subject | GPR4 | en_US |
| DC.subject | CFA | en_US |
| DC.title | 酸敏感G蛋白偶合受體OGR1, G2A, GPR4經由不同方式調控發炎所產生的機械性痛覺敏感現象 | zh_TW |
| dc.language.iso | zh-TW | zh-TW |
| DC.title | OGR1, G2A, and GPR4 regulate mechanical hyperalgesia induced by inflammation via distinct ways | en_US |
| DC.type | 博碩士論文 | zh_TW |
| DC.type | thesis | en_US |
| DC.publisher | National Central University | en_US |