Pretreatment with hydrogen-rich saline reduces the damage caused by glycerol-induced rhabdomyolysis and acute kidney injury in rats.
BACKGROUND
Rhabdomyolysis is a leading cause of acute kidney injury. The pathophysiological process involves oxidative stress and inflammation. Hydrogen-rich saline (HRS) is an antioxidant and anti-inflammatory. This study explored the protective effect of pretreatment with HRS on the development of glycerol-induced rhabdomyolysis acute kidney injury.


METHODS
Forty-eight rats were randomly divided into four equal groups. Group 1 served as the control, group 2 was given 50% glycerol (10 mL/kg, intramuscular), group 3 was given glycerol after 7 d pretreatment with high dose HRS (10 mL/kg/d, intraperitoneal), and group 4 was given glycerol after 7 d pretreatment with low dose HRS (5 mL/kg/d, intraperitoneal). Renal health was monitored by serum creatinine (Cr), urea, and histologic analysis; rhabdomyolysis was monitored by creatine kinase (CK) levels; and oxidative stress was monitored by kidney tissue reactive oxygen species (ROS), malondialdehyde, 8-hydroxydeoxyguanosine (8-OH-dG), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) levels. Inflammation was monitored by interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) evaluation.


RESULTS
Glycerol administration resulted in an increase in the mean histologic damage score, serum Cr, urea and CK, kidney tissue ROS, malondialdehyde, 8-OH-dG, GSH-PX, IL-6, and TNF-α, and a decrease in kidney tissue superoxide dismutase activity. All these factors were significantly improved by both doses of HRS, but the mean histologic damage score, urea, Cr, CK, ROS, 8-OH-dG, GSH-PX, IL-6, and TNF-α for the high dose HRS treatment group were even lower.


CONCLUSIONS
Pretreatment by HRS ameliorated renal dysfunction in glycerol-induced rhabdomyolysis by inhibiting oxidative stress and the inflammatory response.
Department of Nephrology, No.88 Hospital of PLA, Taian, Shandong Province, China.
Hongxia
H
Gu
Department of Nephrology, No.88 Hospital of PLA, Taian, Shandong Province, China.
Min
M
Yang
Institution of Atherosclerosis, Taishan Medical University, Taian, Shandong Province, China.
Xiaomin
X
Zhao
Institution of Atherosclerosis, Taishan Medical University, Taian, Shandong Province, China.
Bing
B
Zhao
Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
Xuejun
X
Sun
Department of Nephrology, No.88 Hospital of PLA, Taian, Shandong Province, China. Electronic address: gaoxinmedsci@163.com.
Xin
X
Gao
D058186:Acute Kidney Injury / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D003402:Creatine Kinase / Q000097:blood; D004195:Disease Models, Animal; D004353:Drug Evaluation, Preclinical; D005990:Glycerol; D006859:Hydrogen / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012206:Rhabdomyolysis / Q000097:blood / Q000139:chemically induced / Q000150:complications*; D012965:Sodium Chloride / Q000494:pharmacology / Q000627:therapeutic use*
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D012965:Sodium Chloride; D006859:Hydrogen; D003402:Creatine Kinase; D005990:Glycerol
Acute kidney injury; Hydrogen-rich saline; Inflammation; Oxidative stress; Rhabdomyolysis