Lysergic acid diethylamide causes mouse retinal damage by up-regulating p-JAK1/p-STAT1.

Purpose: Lysergic acid diethylamide (LSD) is a powerful hallucinogen with high potential for abuse. There is far less known about its effects on the retina, especially the underlying mechanisms. This study was to investigate the acute toxicity of LSD on the retina of C57 mice and its mechanisms of action.Methods: C57 mice were treated with LSD at progressively increasing doses (0.2-1.2 mg/kg) intraperitoneally two times daily for 5 days, mice treated with saline served as negative control. Electroretinography (ERG) was used to test the function of the retina. Toluidine blue staining was used to detect the morphology of the retina. Enzyme-linked immunosorbent assay (ELISA) was used to measure the apoptosis-related factors. Real-time PCR and western blot techniques were used to measure expression changes of genes and proteins, respectively.Results: LSD treatment caused retinal damage, as shown by a decrease in ERG response and the loss of photoreceptor cells. LSD treatment also increased apoptosis through up-regulating the expression of p-JAK1/p-STAT1.Conclusions: Our study indicated that intraperitoneal administration of LSD-induced retinal damage of C57 mice, at least partially through regulating the JAK/STAT pathway.

Astragalus polysaccharide ameliorates ionizing radiation-induced oxidative stress in mice.

Radioprotective compounds from plant resources may represent safe and cost-effective prophylactic and therapeutic agents. This study was designed to investigate the protective effect of polysaccharide derived from the dried roots of the Astragalus spp. (APS) against ionizing radiation (IR) injury in liver and to explore its role in radiation-induced oxidative stress using a mouse model. Prior to (60)Co γ-irradiation (5Gy, single dose), mice received 7 days of APS at low, mid and high doses (50, 100 or 200mg/kg/day, respectively; n=6 each group), vehicle alone (5mL normal saline orally/daily; n=6). A non-irradiated control group (n=6) received the 7-day distilled water regimen only. At 24h post-irradiation, the APS pre-treated mice showed significantly decreased alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase levels, and NF-κB expression. All APS-treated mice also showed attenuation of the IR-induced increase in thiobarbituric acid reactive substance and resolution of the IR-induced decreases in superoxide dismutase, catalase and glutathione activities (all p<0.05). High dose APS pre-treatment led to remarkably less morphologic features of IR-induced hepatic and pulmonary injury. Thus, APS exerts protective effects against IR-induced injury in liver in mice, and the related molecular mechanism may involve suppressing the radiation-induced oxidative stress reaction.