1.Research advances in the role of the cGAS-STING signaling pathway in eye diseases
Yuyu XUE ; Lu YE ; Hejiang YE
Recent Advances in Ophthalmology 2024;44(12):999-1004
The cGAS-STING signaling pathway plays a crucial role in innate immunity,forming a monitoring system for tissue injury and pathogen invasion.Recent studies have found that the cGAS-STING signaling pathway may mediate a vari-ety of pathological processes in eyes and participate in the occurrence and development of inflammatory,degenerative eye diseases and ocular tumors,such as keratitis,age-related macular degeneration,diabetic retinopathy,and uveal melano-ma.This review aims to summarize the role of the cGAS-STING signaling pathway in eye diseases and elucidate the poten-tial molecular mechanisms of the cGAS-STING signaling pathway in eye diseases,so as to provide innovative approaches to the treatment of eye diseases.
2.Application progress of ultrasound-guided genicular nerve block
Jinyan GONG ; Yuyu HAN ; Pengcheng LIU ; Xue YU ; Chengjie GAO ; Yuheng LI ; Fei WANG
The Journal of Clinical Anesthesiology 2024;40(11):1200-1204
Genicular nerve block is usually used for the treatment of chronic pain of knee osteoar-thritis,which can effectively relieve knee pain and preservemotor function.With the rapid development of ultrasound technology,ultrasound-guided genicular nerve block can improve the accuracy of nerve block and reduce block-related complications.This article reviews the research progress of ultrasound-guided genicular nerve block in three aspects:anatomy,operation methods and clinical application.
3.Coptidis Rhizoma Crude Polysaccharide and Berberine Synergistically Restore Intestinal Mucosal Barrier Damage in Ulcerative Colitis
Mingsong XUE ; Yuyu ZHENG ; Yufeng ZHANG ; Quan TAO ; Ye YANG ; Dengke YIN
Chinese Journal of Experimental Traditional Medical Formulae 2022;28(13):71-76
ObjectiveTo investigate the synergistic effect of Coptidis Rhizoma crude polysaccharide (CCP) and berberine (BBR) in treating ulcerative colitis (UC) model mice. MethodThirty male BALB/c mice were randomized into five groups. Except the 6 mice in the normal group, the rest were given 5% dextran sodium sulfate in their daily drinking water to establish the UC model. After modeling, the mice were administrated with corresponding agents by gavage once daily for 4 days: BBR (100 mg·kg-1) group, BBR (100 mg·kg-1) + low-dose (22.8 mg·kg-1) CCP group, BBR (100 mg·kg-1) + high-dose (45.6 mg·kg-1) CCP group. The mice in the model group and normal group were administrated with the same volume of normal saline. At the end of the experiment, the mice were sacrificed for the collection of colon, and the expression of tight junction proteins zonula occluden-1 (ZO-1), Claudin-1, and Occludin in colon tissue was detected by Western blot. With the normal group as the control, the disease activity index (DAI) score, colon length, colon histomorphology, and expression levels of tight junction proteins in other groups were evaluated. ResultCompared with the normal group, the modeling down-regulated the protein levels of ZO-1, Claudin-1, and Occludin (P<0.01). Compared with the model group, BBR did not significantly change the protein level of Claudin-1 and up-regulated those of ZO-1 and occludin (P<0.01). The expression levels of Claudin-1, ZO-1, and Occludin were up-regulated in BBR + CCP groups (P<0.01). The expression levels of tight junction proteins in BBR + CCP groups were significantly higher than those in the BBR group (P<0.05). ConclusionThe administration of CCP combined with BBR can effectively ameliorate intestinal mucosal barrier damage in the mice with UC.
4.Research progress of m6A methylation modification in ocular diseases
Yuyu XUE ; Chunmeng LIU ; Jie CHEN ; Hejiang YE
International Eye Science 2024;24(4):589-595
N6-methyladenosine(m6A), the most common, abundant, and conserved RNA modification in eukaryotic cells, regulates RNA splicing, stability, output, degradation and translation through m6A methyltransferase, m6A demethylase, and m6A methylated binding proteins. Recent studies have found that abnormal m6A methylation may mediate a variety of pathological processes in eyes and participate in the occurrence and development of metabolic, inflammatory, degenerative ocular diseases and ocular tumors, such as diabetic retinopathy, cataract, age-related macular degeneration and uveal melanoma. This review aims to summarize the roles of m6A methylation modification in ocular cells and ocular diseases, elucidate the potential molecular mechanisms of m6A methylation in ocular diseases, so as to encourage innovative approaches in the treatment of these ocular diseases.