Inhibition of mitochondria-dependent apoptosis by 635-nm irradiation in sodium nitroprusside-treated SH-SY5Y cells

Importance of oligodendrocyte protection, BBB breakdown and inflammation for remyelination

“…Nitric oxide (NO) is a diffusible and reactive free radical involved in a variety of physiological functions, including control of the vascular tone, platelet aggregation, and the immune response [40, 41] and a major factor contributing to the loss of neurons in ischemic stroke, demyelinating diseases, and other neurodegenerative disorders [42]. NO is involved in glutamate induced excitation with direct effects on BBB permeability, clearence of CNS inflammation, possibly via induction of encephalitogenic T cell apoptosis, and mediating demyelination, oligodendrocyte destruction and injury to axons [43].…”

“…NO can function as a direct neurotoxin or may react with superoxide (O 2 − ) by a diffusion-controlled reaction to form peroxynitrite (ONOO − ), a species that also contributes to oxidative signaling and cellular apoptosis [42]. However, the mechanism by which ONOO − induces apoptosis remains unclear, although subsequent formation of reactive oxygen species (ROS) such as O2 − , H2O2, OH − , and ONOO − has been suggested [42]. These observations support a potential role of iNOS in initiation of MS lesions.…”

Effects of 635nm light‐emitting diode irradiation on angiogenesis in CoCl2‐exposed HUVECs

“…Some investigators have also suggested that 632.8 nm wavelength irradiation leads to a decrease in intracellular ROS levels, and consequent alleviation of oxidative stress. In a previous report, it was shown that, via promotion of the scavenging of O, light irradiation at 635 nm protects against neuronal death by blocking the mitochondrial apoptotic pathway induced by ONOO − synthesis 28. It has also been reported, in both an in vitro and in vivo model, that low‐level light irradiation alleviates inflammation by inhibiting prostaglandin E 2 production and cyclo‐oxygenase (COX)‐1 and ‐2 mRNA expression 20, 26.…”

Hyperosmolarity‐mediated mitochondrial dysfunction requires Transglutaminase‐2 in human Corneal epithelial cells

“…Mitochondria provide energy for cellular activities (Niizuma et al, 2009) and play an essential role in apoptotic signal transduction. Its normal functioning and energy production depends on the action of both pro-and anti-apoptotic Bcl-2 family proteins and their interaction at the mitochondrial membrane (Hazlett, 2007;Niswander and Dokas, 2007;Lim et al, 2009;Szegezdi et al, 2009). Mitochondria have been implicated in corneal epithelial cell death as evidenced by cytochrome C release (Luo et al, 2004).…”