In contrast, similar to replication enhancing mutations which lower or even prevent secretion of HCV core protein from Con1-transfected cells, incubation with BAs slightly decrease core release. Nevertheless, at least for the K1846T-adapted genome addition of CDCA slightly increased the number of detectable HCV infected cells. In the future it will be interesting to find out if replication of viral genomes from different viral genotypes is also stimulated by BAs and by which mechanism and extent these compounds facilitate HCV RNA-replication. In this regard the moderate stimulatory effect of BAs on replication of wild type full length HCV genomes may facilitate the identification of novel primary isolates that are replication competent in cell culture. Considering that during bile duct obstructions serum levels of BAs ranging up to 400 mM are reached, endocrine functions of BAs may in these patients at least transiently modulate virus replication. This in turn may influence treatment response and the ability of the virus to acquire drug resistance and should be considered when tailoring optimal treatment for patients with these complications. Photoreceptor loss occurs acutely after retinal detachment. Although surgery is performed for rhegmatogenous retinal detachment the visual acuity of patients is not always restored after successful reattachment surgery. In other retinal disorders Angoroside-C including age-related macular degeneration and diabetic retinopathy, retinal photoreceptor detachment persists chronically and vision loss progresses for many patients. Studies in humans and in experimental animal models have demonstrated that after detachment of the retina, the photoreceptors begin to degenerate and die over time. Therefore, therapeutic agents targeting photoreceptor death may improve treatment for retinal disorders associated with retinal detachment. TUDCA is a minor component of human bile and a primary constituent of bear bile. Bear bile has been used in Chinese medicine for ophthalmic and hepatic indications for over 3000 years. Recently, researchers have tested TUDCA and related bile acids for biological activity using modern scientific methods. The related drug, ursodeoxycholic acid -also known as Actigall, Urso, or Ursodiol- reduces liver damage in the setting of cholestasis and has been approved by FDA for the treatment of Harpagoside biliary cirrhosis. TUDCA itself has been demonstrated to show cytoprotective effects in a variety of experimental systems including several models of neurodegenerative diseases as well as against light-induced or oxidative stress-induced retinal damage in mice and mouse model of retinitis pigmentosa. This study tests whether the systemic administration of tauroursodeoxycholic acid can protect photoreceptors from cell death after experimental retinal detachment. We show that this agent has neuroprotective effects, associated with inhibition of apoptosis and decrease in oxidative stress, thereby exhibiting potential as a novel neuroprotective therapeutic drug in eye diseases characterized by photoreceptor cell loss due to retinal detachment. Hydrophilic bile acids like UDCA and TUDCA had been empirically used for ophthalmic indications in traditional Chinese medicine for thousands of years. Recently they have been studied more systematically and have been shown to be cytoprotective in experimental models of neurodegenerative diseases, including Huntington’s disease, Alzheimer’s disease, Parkinson’s disease and hemorrhagic stroke. In mice, TUDCA also protects photoreceptors against light-induced retinal damage and from a genetic mutation that models retinitis pigmentosa. In this study, we demonstrate that systemic administration of the hydrophilic bile acid TUDCA has photoreceptor neuroprotective effects in an experimental retinal detachment model and in agreement with studies by others, where TUDCA has been shown to mediate its cytoprotective effects partially through inhibition of caspase mediated apoptosis.