Lutein Attenuates Both Apoptosis and Autophagy upon Cobalt (II) Chloride-Induced Hypoxia in Rat Műller Cells

Abstract

Retinal ischemia/reperfusion injury is a common feature of various retinal diseases such as glaucoma and diabetic retinopathy. Lutein, a potent anti-oxidant, is used to improve visual function in patients with age-related macular degeneration (AMD). Lutein attenuates apoptosis, oxidative stress and inflammation in animal models of acute retinal ischemia/hypoxia. Here, we further show that lutein improved Műller cell viability and enhanced cell survival upon hypoxia-induced cell death through regulation of intrinsic apoptotic pathway. Moreover, autophagy was activated upon treatment of cobalt (II) chloride, indicating that hypoxic injury not only triggered apoptosis but also autophagy in our in vitro model. Most importantly, we report for the first time that lutein treatment suppressed autophagosome formation after hypoxic insult and lutein administration could inhibit autophagic event after activation of autophagy by a pharmacological approach (rapamycin). Taken together, lutein may have a beneficial role in enhancing glial cell survival after hypoxic injury through regulating both apoptosis and autophagy.

Cytoprotective Effects of Natural Highly Bio-Available Vegetable Derivatives on Human-Derived Retinal Cells

“…Given the crucial role played by autophagy in the RPE, alteration of the autophagy flux could have deleterious consequences for the cells, including accumulation of toxic compounds (i.e., vacuoles containing undigested materials, oxidized compounds, aggregates, and damaged organelles) and uncontrolled inflammation, which are conditions contributing to retinal degeneration. Data from the literature indicate that lutein and curcumin can modulate autophagy [12,38,72]. Our data suggest that lutein, and potentially curcumin can prevent autophagy flux alteration induced by blue LED exposure.…”

“…Moreover, lutein and zeaxanthin exert neuroprotective effects in vision-threatening diseases, such as innate retinal inflammation, diabetic retinopathy, and participation in the development and/or maintenance of the RPE, which could thereby reduce susceptibility to macular degeneration [11]. Recently, lutein has been shown to modulate autophagy [12], an intracellular degradation system that delivers cytoplasmic constituents to the lysosome [13]. Autophagy mediates numerous cytoprotective effects [14].…”

Lutein and the Aging Eye

“…Our data revealed that lutein could protect ganglion cells from either H 2 O 2 -induced oxidative stress or CoCl 2 (cobalt chloride)-induced chemical hypoxia [39]. Moreover, in the treatment of CoCl 2 on Müller cells, lutein not only improved cell viability and enhanced cell survival but also inhibited the formation of autophagosome [40]. In the rat model of retinal detachment, lutein preserved cells in ONL and rhodopsin expression, indicating its neuroprotective and anti-apoptotic effects [41].…”

Cobalt chloride affects the death of SH-SY5Y cells induced by inhibition of ubiquitin proteasome system. Role of heat shock protein 70 and caspase 3

“…Previous studies have demonstrated mitochondrial dysfunction and transmembrane potential collapse caused by opening the mitochondrial transition pore and inhibition of the mitochondrial respiratory chain complexes (Battaglia et al 2009). In addition, induction of apoptosis (Yang et al 2004;Jung et al 2007;Walls et al 2009;Chang et al 2016) autophagy (Yang et al 2015;Fung et al 2016) and oxidative stress Stenger et al 2011;Guan et al 2015) has also been documented among the mechanisms of Co 2+ -induced cell death.…”