Coumestrol inhibits inflammation, apoptosis and oxidative stress in
retinal cells of diabetic retinopathy rats by SIRT1 Running title: CMS
& SIRT1 on DR rats
Diabetes-induced oxidative stress is the key factor that initiates
neuronal damage in the diabetic retina leading to diabetic retinopathy.
This study was to investigate the possible effects of coumestrol (CMS)
on inflammation, apoptosis and oxidative stress of retinal cells in
streptozotocin-nicotinamide (STZ)-induced DR. Initially, a rat model of
STZ was established by intraperitoneal injection of streptozotocin, and
the expression of SIRT1 in retina tissues was determined by RT-qPCR.
Next, the regulatory roles of CMS in oxidative stress, inflammation, and
apoptosis of retinal cells were analyzed through detecting the
expression of ROS, MDA, SOD, NO, iNOS, IL-6, TNF-α, and CRP, apoptotic
factors (Cyt-C and Caspase-3) after ARPE-19 cells were treated with CMS.
Moreover, the relationship between CMS and SIRT1 was analyzed. SIRT1 was
lowly expressed in retina tissues. CMS treatment suppressed expression
of ROS, MDA, iNOS, NO, IL-6, TNF-α, and CRP, as well as expression of
Cyt-C and Caspase-3, but induced SOD expression in retina cells. CMS
activated the expression of SIRT1, thereby inhibited oxidative stress,
inflammation and apoptosis of retinal cells induced by DR. Taken
together, the present study defines that CMS ameliorated DR by
inhibiting inflammation, apoptosis and oxidative stress of retinal cells
through the activation of SIRT1.