RESUMO
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.
Assuntos
Alucinógenos/toxicidade , Janus Quinase 1/metabolismo , Dietilamida do Ácido Lisérgico/toxicidade , Retina/efeitos dos fármacos , Fator de Transcrição STAT1/metabolismo , Animais , Eletrorretinografia , Feminino , Camundongos Endogâmicos C57BL , Retina/metabolismo , Retina/patologia , Retina/fisiopatologia , Doenças Retinianas/induzido quimicamente , Doenças Retinianas/metabolismo , Doenças Retinianas/patologia , Doenças Retinianas/fisiopatologia , Regulação para Cima/efeitos dos fármacosRESUMO
AIM: To investigate the chronic effect of palmitic acid (PA) on apoptosis of pancreatic islet beta-cells and the possible mechanism. METHODS: Insulinoma cell line (MIN6 cells) were used in this study. After being incubated in PA (0.1 - 1.6 mml/L) for 24 and 48 hours, MTT method was used to evaluate the livability. After being incubated for 48 h, Hoechst-PI and Annexin-V-FTTC/PI FACS were used to estimate the apoptosis in each group, Western-blotting assay was used to estimate the protein level of p-Akt, Akt, Bax and Bcl-2. RESULTS: Chronic PA dose-dependently (1) decreased the availability and increased the apoptosis of MIN6 cells; (2) decreased the phosphorylation of Akt and Bcl-2, but had no significant effects on Akt and Bax. CONCLUSION: Chronic PA dose-dependently induced apoptosis of MIN6 cells, and this effect was possibly regulated by Akt/Bcl-2.