Curcumin regulates intracellular calcium release and inhibits oxidative stress parameters, VEGF, and caspase-3/-9 levels in human retinal pigment epithelium cells

Abstract

In this study, we aimed to observe whether curcumin (cur), a polyphenolic compound derived from the dietary spice turmeric, a yellow substance obtained from the root of the plant Curcuma longa Linn, has any protective effect against blue light irradiation in human retinal pigment epithelium (ARPE-19) cells. For this purpose, we evaluated the intracellular calcium release mechanism, poly ADP ribose polymerase (PARP), procaspase-3/-9 protein expression levels, caspase activation, and reactive oxygen species levels. ARPE-19 cells were divided into four main groups, such as control, cur, blue light, and cur + blue light. Results were evaluated by Kruskal-Wallis and Mann-Whitney U tests as post hoc tests. The cells in cur and cur + blue light samples were incubated with 20 μM cur. Blue light exposure was performed for 24 h in an incubator. Lipid peroxidation and cytosolic-free Ca [Ca] concentrations were higher in the blue light exposure samples than in the control samples; however, their levels were determined as significantly lower in the cur and cur + blue light exposure samples than in the blue light samples alone. PARP and procaspase-3 levels were significantly higher in blue light samples. Cur administration significantly decreased PARP and procaspase-3 expression levels. Reduced glutathione and glutathione peroxidase values were lower in the blue light exposure samples, although they were higher in the cur and cur + blue light exposure samples. Caspase-3 and -9 activities were lower in the cur samples than in the blue light samples. Moreover, vascular endothelial growth factor (VEGF) levels were significantly higher in the blue light exposure samples. In conclusion, cur strongly induced regulatory effects on oxidative stress, intracellular Ca levels, VEGF levels, PARP expression levels, and caspase-3 and -9 values in an experimental oxidative stress model in ARPE-19 cells.

Reactive Oxygen Species Regulate Endoplasmic Reticulum Stress and ER‐Mitochondrial Ca2+ Crosstalk to Promote Programmed Necrosis of Rat Nucleus Pulposus Cells under Compression

“…Ca 2+ overload in the mitochondria usually serves as intracellular signaling for PARP activation [35,36]. PARP activation leads to PARP-mediated mitochondrial dysfunction, as demonstrated by mitochondrial membrane depolarization, overproduction of superoxide, and loss of cardiolipin content [37].…”

Deletion of Mitochondrial Translocator Protein (TSPO) Gene Decreases Oxidative Retinal Pigment Epithelial Cell Death via Modulation of TRPM2 Channel

“…Inactive forms of Casp -3 and Casp -9 locate in cytoplasm of cells, including ARPE19 [ 38 , 39 ]. In the pathways of apoptosis, Casp -3 and Casp -9 proteins have key roles.…”

“…TRPM2 and the absence of currents in the ARPE19-KO obviously evidenced the involvement of TPSO on TRPM2 activation in the ARPE19. Inactive forms of Casp -3 and Casp -9 locate in cytoplasm of cells, including ARPE19 [38,39]. In the pathways of apoptosis, Casp -3 and Casp -9 proteins have key roles.…”

Curcumin enhances cisplatin-induced human laryngeal squamous cancer cell death through activation of TRPM2 channel and mitochondrial oxidative stress

“…In the patch-clamp experiments and laser confocal microscope analyses, we have observed increased levels of TRPM2 current density and Ca 2+ fluorescence intensity through oxidative stress (CPx) stimulation in Hep2 cells, but their density and intensity were decreased by TRPM2 channel blockers (ACA and 2-APB) in Hep2 cells. In recent studies, the protective role of CURC through the inhibition of TRPM2 channel were reported against excessive Ca 2+ entry into cytosol of different normal cells 29,30,33–36 . However, accumulating evidence indicates that CURC has also pro-oxidant and calcium channel activating actions 20,21,37,38 .…”