Carnosine improves diabetic retinopathy via the MAPK/ERK pathway.

Diabetic retinopathy (DR) is one of the most common causes of blindness in developed countries. Due to its asymptomatic onset and progressive disease course, DR is typically diagnosed at a late stage when treatment options are limited and therefore often results in irreversible blindness. Studies have demonstrated that carnosine may prevent and treat DR. In a previous study, the positive effect of carnosine on DR was determined and it was revealed that there may be an association between carnosine and the mitogen-activated protein kinase (MAPK)/extracellular signal related kinase (ERK) signaling pathway. To assess the interaction between carnosine and the MAPK/ERK signaling pathway, changes in PKC, ERK and p-ERK expression was assessed in diabetic rats following treatment with carnosine, PD98059 or U46619 via reverse transcription-quantitative polymerase chain reaction and western blotting. The results demonstrated that the expression of ERK and p-ERK were significantly suppressed following treatment with carnosine, but no significant effect on the expression of PKC was identified, which indicates that suppressing the activation of the MAPK/ERK signaling pathway may serve an important role in carnosine-induced DR prevention and treatment.

Factors correlated with the resolution of macular oedema after one dose injection of intravitreal triamcinolone acetonide treatment in branch retinal vein occlusion.

OBJECTIVE: To investigate the predictive baseline factors for a successful outcome following one dose of intravitreal triamcinolone acetonide (IVTA) in patients with macular oedema (ME) caused by branch retinal vein occlusion (BRVO). METHODS: This retrospective study enrolled patients with ME (macular retinal thickness [MRT] ≥ 300 µm) due to BRVO who still had ME 3 months after grid laser photocoagulation. Patients were divided according to treatment into an IVTA group and a laser-only group. The resolution of ME was documented at months 3 and 6. RESULTS: A total of 154 eyes with ME were investigated: IVTA group (90 eyes) and laser-only group (64 eyes). Predictive factors for successful IVTA treatment were younger age, shorter duration of ME, initial onset ME, accompanied by serous retinal detachment, few concomitant systemic diseases and nonischaemic BRVO. A broken foveal capillary ring was related to a poor treatment outcome. Eyes with cystoid spaces in the outer plexiform layer were more likely to have a good treatment response. CONCLUSION: IVTA is effective for resolving ME due to BRVO after grid laser photocoagulation treatment.

Effect of carnosine, aminoguanidine, and aspirin drops on the prevention of cataracts in diabetic rats.

PURPOSE: To investigate the effect of carnosine (CA), aminoguanidine (AG), and aspirin (ASA) drops, all inhibitors of glycation, on the development of diabetic cataract in rat. METHODS: Rats were made diabetic with streptozotocin, and based on the level of plasma glucose, they were assigned as non-diabetic rats (<14 mmol/l plasma glucose) and diabetic rats (>14 mmol/l plasma glucose). Animals in the treated groups received CA, AG, and ASA as drops to the left eyes starting from the day of streptozotocin injection. Progression of lens opacification was recorded using the slit lamp at regular time intervals. All the rats were killed after the week 13, and the levels of advanced glycation end products (AGE), glutathione reductase (GR), catalase (CAT), and glutathione (GSH) were determined. RESULTS: Lens opacification progressed in a biphasic manner in the diabetic rats, an initial slow increase during the first eight weeks of diabetes followed by a steep increase in the next five weeks. Carnosine treatment delayed the progression of cataracts in diabetic rats, and the delay was statistically significant on the fourth week of diabetes (p<0.05, when compared with untreated moderately diabetic rats). A decrease in the antioxidant enzymes of CAT and the level of GSH was found in the lens of the untreated diabetic rats at 13 weeks after injection. Some protection was provided in the treated eyes. The level of glycation in the untreated diabetic rats was significantly higher than that in the normal rats (p<0.001). After treatment with CA, AG, and ASA, those diabetic rats had a lower level of glycated lens protein compared to the untreated diabetic rats (p<0.001). CONCLUSIONS: These results thus suggest that the effect of CA, AG, and ASA is indeed inhibition of the formation of AGEs. However, the effect of CA, AG, and ASA is overwhelmed by the excessive accumulation of AGEs in the severely diabetic rats. CA compared with AG and ASA treatment can delay the progression of lens opacification in the diabetic rats only during the earlier stages. It also protects against the inactivation of enzymes.