ABSTRACT
Macular edema is formed by the accumulation of extracellular fluid or intracellular fluid in the macular area of the retina. In a physiological state, the retina is kept relatively dehydrated and transparent, thereby ensuring the transmission of optical signals. This process requires multiple active or passive liquid transport systems to be performed together, and any of these process anomalies can disrupt the retinal water ion homeostasis, causing an imbalance between fluid entry and exit processes, leading to fluid formation. Macular edema is not an independent disease, it can occur in the process of many retinal diseases. It is the main cause of serious damage to the central vision, the main causes of diabetes, retinal vein occlusion, choroidal angiogenesis, uveitis, postoperative inflammation and tumor. This review mainly discusses the complex mechanism of macular edema caused by retinal barrier dysfunction when retinal water ion homeostasis is abnormal at the cellular and molecular levels. The purpose of this review is to provide a deeper overview of macular edema and its mechanisms of development, opening up new prospects for new prevention and treatment strategies for macular edema, a serious threat to vision.
ABSTRACT
Objective To study the interference effects of tetramethylpyrazine (TMP) on calcinuerin (CaN), c-fos and the nuclear antigen of proliferating cells in the proliferation of vascular smooth muscle cells (VSMCs) treated by angiotensinⅡ(Ang Ⅱ). Methods A cell proliferating model of VSMCs induced by Ang Ⅱ was established; the effects of TMP on CaN was detected by enzyme reaction phosphorus measurement; the effects of TMP on c-fos gene and PCNA expression were observed by immunocytochemical staining and image analysis technique (A value). Results The rats’ aortic smooth muscle cells were cultured in vitro successfully. CaN activities, cell proliferation activity and the expression levels of c-fos and PCNA increased significantly in VSMCs proliferation induced by Ang Ⅱ (P