Carvedilol promotes retinal ganglion cell survival following optic nerve injury via ASK1-p38 MAPK pathway.

Carvedilol promotes retinal ganglion cell survival following optic nerve injury via ASK1-p38 MAPK pathway. CNS Neurol Disord Drug Targets. 2019 Oct 01;: Authors: Liu B, Liu YJ Abstract Carvedilol, which is considered as a nonselective β-adrenoreceptor blocker, has many pleiotropic activities. It also causes great influence on neuroprotection because of its antioxidant ability. It is shown in this research that carvedilol could cause influence on preventing retinal ganglion cell (RGC) death caused by optic nerve injury (ONI) as an experimental model. RGC death after ONI could be decreased following carvedilol treatment. And in vivo retinal imaging revealed that carvedilol can effectively prevent retinal degeneration. Moreover, it was demonstrated that carvedilol inhibited ONI-induced expression of chemokines necessary for microglia recruitment and, consequently, accumulation of retinal microglia was reduced. The production of inducible nitric oxide synthase was inhibited with carvedilol treatment in the retina. We also discovered that carvedilol suppressed ONI-induced activation of apoptosis signal-regulating kinase-1 (ASK1) and p38 mitogen-activated protein kinase (MAPK). The results of this study demonstrate that carvedilol has a role in neuroprotection and neuroregeneration, and may be useful in neurodegenerative diseases treatment. PMID: 31577210 [PubMed - as supplied by publisher]
Source: CNS and Neurological Disorders Drug Targets - Category: Drugs & Pharmacology Authors: Tags: CNS Neurol Disord Drug Targets Source Type: research