Effect of luteoin in delaying cataract in STZ-induced diabetic rats.

Luteolin, a flavonoid rich in many plants, has shown various pharmacological effects including anti-inflammation, anti-oxidant, anti-tumor, cardioprotective and neuroprotective properties. At present, inflammation and oxidative stress have been recognized to be two important contributing factors to the development of diabetic cataract. The aim of this study is to investigate the effects of luteolin on diabetes-induced oxidative stress and inflammation in the lens of rats. A diabetic rat model was induced by intraperitoneally giving streptozotocin at a dosage of 60 mg/kg, and then the rats were treated by orally administration of luteolin 25, 50 and 100 mg/kg for 12 weeks. The results showed that luteolin administration could increase the antioxidant capacity such as glutathione (GSH) and glutathione peroxidase (GPx) activity, and decreased malondialdehyde (MDA) level in the lens of diabetic rats. Luteolin also inhibited diabetes-induced elevation of interleukin-1 beta (IL-1ß), vascular endothelial growth factor and nuclear factor-κB (NF-κB) mRNA and protein expression in lens. Moreover, in the high dose group (100 mg/kg), lens GSH level was decreased to normal compared to control group. The degree of oxidative and inflammatory damage was significantly reduced in luteolin-treated rats. These data suggested that luteolin can be an effective protection candidate of diabetes-induced lens neurodegeneration by inhibiting the levels of inflammatory mediators and oxidative stress.

Effect of lithium chloride on endoplasmic reticulum stress-related PERK/ROCK signaling in a rat model of glaucoma.

Elevated intraocular pressure (IOP) is considered as the major risk factor for the loss of retinal ganglion cells (RGCs) and their axons in glaucoma. Lithium chloride (LiCl) inhibits glycogen synthase kinase-3 beta (GSK-3ß) and attends PERK-induced endoplasmic reticulum stress (ERs) transition. PERK is a type I transmembrane protein located in the endoplasmic reticulum. PERK pathway activation takes place in ERs early inhibiting protein synthnesis to protect cell and promote cell survival. Here, we firstly evaluate that LiCl reduced IOP when administered intraperitoneally. After 6 weeks, IOP dropped by around 21.9% in LiCl treated rats. Then we investigated the effects of LiCI on PERK-mediated signaling pathways. LiCl treatment activated PERK and inhibited the expression of ROCK-1 and ROCK-2 in a rat model of glaucoma. Collectively, these results suggest that LiCl reduced the IOP through the phosphorylation of PERK by the regulation of PERK/ROCK signaling in glaucoma rat model.