RESUMO
Background Glial scaring induced by the activation and proliferation of astrocytes after optical nerve damage is one of causes of neural axons difficult to regeneration.Researches showed that α-crystallin can promote the regeneration and pass through scaring zone of retinal ganglion cells (RGCs) axons,and we speculate α-crystallin protect optical nerve tissue against scaring process.Objective This study was to investigate the influence of α-crystallin for the activation and secretion of inflammatory factors of astrocytes.Methods Optical nerver tissue was isolated from 3-5 day-old SPF Long Evans rats to culture and purify astrocytes.The cells were identified by detecting the expression of glial fibrillary acidic protein (GFAP) with immunofluorescence technique.The cells were cultured with regular culture medium in the normal control group,and 5 μg/ml lipopolysaccharides (LPS) was added in the LPS group,while 5 μg/ml LPS and 1 ×10-4 g/L α-crystallin were added in the α-crystallin group,and the cells were consecutively cultured for 24 hours.The proliferation (absorbance,A) of the cells was assayed by cell counting kit-8 (CCK-8).The expression of GFAP in the cells was detected by immunofluorescence technique and quantitated by Western blot.The contents in the cell supernatants of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected by ELISA.Results The morphology and size were well-proportioned in 3-4 generation of cells with the GFAP positive rate over 95％.The A values were 1.335±0.070,1.643±0.069 and 1.390±0.004 in the normal control group,LPS group and α-crystallin group,and the A values in the LPS group were significantly higher than those in the normal control group and α-crystallin group (t =3.315,3.681,both at P＜0.05).Immunofluorescence examination showed that the fluorescence intensity was evidently enhanced in the LPS group compared with the normal control group and α-crystallin group and presented the largest cell bodies in the LPS group.The relative expressions of GFAP in the cells were 0.851 ±0.076 in the LPS group,which were higher than those in the normal control group and α-crystallin group (0.786±0.091,0.569±0.049).Compared between the LPS group and α-crystallin group,there is a significant difference between the two groups (t =3.115,P＜ 0.0l).In addition,compared with the LPS group,the contents of TNF-α and IL-1β in the suspensions were significantly reduced in the normal control group and α-crystallin group (all at P＜0.05).Conclusions α-Crystallin protein can inhibit the activation and secretion of optic nerve astrocytes stimulated by LPS.
RESUMO
This study aimed to determine whether taurine supplementation improves metabolic disturbances and diabetic complications in an animal model for type 2 diabetes. We investigated whether taurine has therapeutic effects on glucose metabolism, lipid metabolism, and diabetic complications in Otsuka Long-Evans Tokushima fatty (OLETF) rats with long-term duration of diabetes. Fourteen 50-week-old OLETF rats with chronic diabetes were fed a diet supplemented with taurine (2%) or a non-supplemented control diet for 12 weeks. Taurine reduced blood glucose levels over 12 weeks, and improved OGTT outcomes at 6 weeks after taurine supplementation, in OLETF rats. Taurine significantly reduced insulin resistance but did not improve beta-cell function or islet mass. After 12 weeks, taurine significantly decreased serum levels of lipids such as triglyceride, cholesterol, high density lipoprotein cholesterol, and low density lipoprotein cholesterol. Taurine significantly reduced serum leptin, but not adiponectin levels. However, taurine had no therapeutic effect on damaged tissues. Taurine ameliorated hyperglycemia and dyslipidemia, at least in part, by improving insulin sensitivity and leptin modulation in OLETF rats with long-term diabetes. Additional study is needed to investigate whether taurine has the same beneficial effects in human diabetic patients.