Does green tea (Camellia sinensis, CS) present neuroprotector effect in the pathogenesis of diabetic retinopathy? In vitro studies in primary rat Muller cell culture to investigate the possible molecular mechanisms involved in neuroprotective effects of CS

Abstract

Diabetic retinopathy (DR) is the leading cause of blindness in developed countries. DR is considered a neurodegenerative disease accompanied by extensive vascular changes. Before the first vascular abnormality is observed, the glial and neural cells are affected by hyperglycemia. The glial cells, mainly the Muller cell, Müller cells, the main glial cells within the retina, are vital for maintaining the normal health of the retina and have been implicated in many retinal diseases, including DR. Glutamate is the main excitatory neurotransmitter in the mammalian brain and retina, but it is neurotoxic when present in excessive amounts. In the retina, glutamate is the primary excitatory transmitter in the vertical pathway from photoreceptors to ganglion cells. A decrease in the ability of Müller cells to remove glutamate from the extracellular space may play a crucial role in the disruption of glutamate homeostasis that occurs in the diabetic retina. Several recent studies have shown that a significant increase in glutamate in the retina is associated with the development of diabetic retinopathy (DR), a disease characterized by neurodegeneration and vasculopathy. Although the detailed mechanism remains unknown, it may be of critical importance for neuroprotection to remove excess glutamate from the extracellular space in the retina.The green tea (GT) (Camellia sinensis) is a functional food. Epidemiological studies have demonstrated a beneficial effect of green tea to cardiovascular protection. The maiority of the gree tea effects are attributed to poliphenols. The poliphenols are 40% of dry weigh of GT and have rised much interest. Evidences suggest neuroprotection of poliphenols through H radicals donation and modulation of caspases via, resulting in protection of neural cells against apoptotic death. The in vitro studies with primary neuronal cells, the treatment with epichatechin (poliphenol) upregulated intracellular signaling, increasing the CREB, ERK and Akt resulting in increase expression of GluR2 receptor. These findings reveal the potetial of poliphenols in modulate neurotransmissors and sinaptogenesis. In visual and ophthalmology research, there is very little information in regard the possible therapeutic effect of poliphenols. The present project aims to investigate the neuroprotective effects of poliphenols in primary culture cell of rat Muller cells in normal and high glucose medium with and without treatment with extract of GT. These studies may provide new therapeutic tolls for the treatment of diabetic retinopathy. (AU)