前列腺素E2在斑馬魚酸鹼調節之功能

Abstract

前列腺素E2(Prostaglandin E2)對於魚類酸鹼平衡的調節仍是未知的。PGE2可透過四型受體(EP)，進而影響不同的生理功能。哺乳類主要利用腎臟維持酸鹼平衡，曾有研究發現PGE2參與兔子集尿管的排酸機制，而兩生類也需要透過表皮組織進行酸鹼平衡，排酸能力會受到不同的PGE2濃度而有所改變。然而，生活在水中的魚類，所需要面對環境改變的壓力比起前兩者更大，為了解PGE2與魚類酸鹼調節之間的關係，本研究將斑馬魚進行七天酸處理後發現鰓上PGE2相關的基因表現量上升。此外，將PGE2合成酵素弱化後，排酸能力、HR細胞數量以及排酸相關蛋白質的基因表現量上升。而將受體的基因ptger1a或ptger1b弱化後，在酸性環境下，可能藉由降低碳酸酐酶(ca2)基因表現量進而導致排酸能力無法上升。由此可知，PGE2可能參與斑馬魚的排酸機制，且在正常環境中的運作機制與酸性環境可能不同。

How PGE2 regulate the acid-base regulation mechanism in fishes is unclear so far. It has been known that PGE2 regulates physiological function via four EP receptors (EP). One of the organs that could regulate acid-base balance in mammalian is the kidney. Previous study found that PGE2 inhibits proton secretion in medullary collecting duct of rabbits. On the other hand, in amphibians, PGE2 maintains the acid-base balance by utilizing epithelium and their proton secretion capability is dependent on the concentration of PGE2. However, Fishes, living in water, have to face stronger stress of environmental pH changes than previous species, especially in fresh water. In order to understand how does PGE2 affect proton secretion in fishes, we use zebrafish as a model animal. The acidic environmental acclimation of adult zebrafish found the up-regulation of PGE2 related genes in the gill. Additionally, knockdown PGE2 synthase (ptges) increases proton secretion ability, H+-ATPase rich (HR) cell number, and the expression of proton secretion related transporter genes were also up-regulated in zebrafish embryos. Furthermore, knockdown ptger1a or ptger1b showed lower proton secretion in acidic environment, it might caused by the down-regulation of ca2. Taken all together, PGE2 might involves in the machinery of acid-base regulation, however, it probably has different regulatory mechanisms between normal and acidic environment in zebrafish.