Protective Effects of Salidroside on Mitochondrial Functions against Exertional Heat Stroke-Induced Organ Damage in the Rat

Abstract

Exertional heat stroke (EHS) results in a constellation of systemic inflammatory responses resulting in multiorgan failure and an extremely high mortality. The present study was designed to evaluate the protective effects of salidroside on EHS by improving mitochondrial functions in the rat model. Liver and heart mitochondria were observed by transmission electron microscopy and mitochondrial membrane potential (ΔΨm) was detected by a fluorescent probe. Intramitochondrial free Ca2+ concentration, mitochondrial respiratory control ratio (RCR), reactive oxygen species (ROS) levels, superoxide dismutase (SOD), and malondialdehyde (MDA) activity were detected by the corresponding kits. RT-PCR was performed to estimate peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and manganese form of SOD (MnSOD) mRNA expression. The results demonstrated that salidroside was able to relieve EHS damage by reducing the swelling of mitochondria, ROS levels, and MDA activity, as well as increasing ΔΨm, RCR, free Ca2+ concentration, SOD, PGC-1α, and MnSOD mRNA levels. In conclusion, salidroside has protective effects on mitochondrial functions against exertional heat stroke-induced organ damage in the rat.

Neuroprotective Effects of Salidroside in the MPTP Mouse Model of Parkinson’s Disease: Involvement of the PI3K/Akt/GSK3βPathway

“…Salidroside (Sal, 2-(4-hydroxyphenyl)ethyl β -D-glucopyranoside, C 14 H 20 O 7 ) is mainly extracted from Rhodiola rosea L., which grows at high altitude localities and usually is used as one of the herbal drugs in worldwide [ 20 ]. Sal has been shown to have numerous pharmacological effects, such as antioxidant effects [ 21 , 22 ], antiapoptosis effects [ 23 ], and maintenance of mitochondrial function [ 24 ]. Our paper recently found that Sal protected DA neurons against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-)/1-methyl-4-phenyl-pyridinium- (MPP + -) induced toxicity in a dose-dependent manner through modulation of the ROS-NO related mitochondrial pathway both in vivo and in vitro [ 25 ].…”

Time-dependent effects of late-onset dietary intake of salidroside on lifespan and age-related biomarkers of the annual fish Nothobranchius guentheri

“…Dietary intake of SDS has been shown to protect PC12 cells against H 2 O 2 -induced apoptosis [ 33 ] and HaCAT cells against UVB-mediated oxidative damage [ 34 ]. SDS has also been reported to alleviate oxidative stress in the liver with non-alcoholic steatohepatitis in rats [ 35 ], to prevent kainic acid-induced status epilepticus via suppressing oxidative stress and diabetes-induced oxidative stress in mice [ 36 , 37 ], and to protect mitochondria against exertional heat stroke-induced organ damage and retinal endothelial cells against hydrogen peroxide-induced injury via modulating oxidative status and apoptosis in rats [ 38 , 39 ]. The main findings of our study are that late-onset SDS administration does not reduce the body weight and length of aging N. guentheri , but it is able to decrease the age-related markers and increase the median and maximum lifespans of the fish.…”

Allicin protects against H2O2-induced apoptosis of PC12 cells via the mitochondrial pathway

“…Cyt C is then translocated into the cytosol and caspase-3/9 is activated to induce cell apoptosis ( 33 , 34 ). The depolarization of ∆ψm, mitochondria swelling, the increase of malondialdehyde and ROS, and the decrease of superoxide dismutase are the characteristics of mitochondrial dysfunction ( 35 ). Zhu et al have demonstrated that allicin provides protection against spinal cord ischemia/reperfusion injury in rabbits through enhancing antioxidant enzyme activities and improving mitochondrial function ( 36 ).…”