Abstract
BackgroundAnisodamine is used for the treatment of reperfusion injury in various organs. In this study, we investigated the effectiveness and mechanisms of action of anisodamine in promoting recovery from glycerol-induced acute kidney injury (AKI).MethodsWe compared the protective effects of atropine and anisodamine in the rat model of glycerol-induced AKI. We examined signaling pathways involved in oxidative stress, inflammation and apoptosis, as well as expression of kidney injury molecule-1 (KIM-1). Renal injury was assessed by measuring serum creatinine and urea, and by histologic analysis. Rhabdomyolysis was evaluated by measuring creatine kinase levels, and oxidative stress was assessed by measuring malondialdehyde (MDA) and superoxide dismutase (SOD) levels in kidney tissues. Inflammation was assessed by quantifying interleukin 6 (IL-6) and CD45 expression. Apoptosis and necrosis were evaluated by measuring caspase-3 (including cleaved caspase 3) and RIP3 levels, respectively.ResultsGlycerol administration resulted in a higher mean histologic damage score, as well as increases in serum creatinine, urea, creatine kinase, reactive oxygen species (ROS), MDA, IL-6, caspase-3 and KIM-1 levels. Furthermore, glycerol reduced kidney tissue SOD activity. All of these markers were significantly improved by anisodamine and atropine. However, the mean histologic damage score and levels of urea, serum creatinine, creatine kinase, ROS and IL-6 were lower in the anisodamine treatment group compared with the atropine treatment group.ConclusionPretreatment with anisodamine ameliorates renal dysfunction in the rat model of glycerol-induced rhabdomyolytic kidney injury by reducing oxidative stress, the inflammatory response and cell death.
Highlights
Anisodamine is used for the treatment of reperfusion injury in various organs
Observation of kidney morphology after glycerol/ anisodamine/atropine treatment Histopathological analysis of kidney tissue was performed after glycerol administration
Pathological changes gradually increased in the acute kidney injury (AKI) group from 3 to 72 h, including tubular epithelial cell swelling, vacuolar degeneration, necrosis and desquamation
Summary
Anisodamine is used for the treatment of reperfusion injury in various organs. We investigated the effectiveness and mechanisms of action of anisodamine in promoting recovery from glycerolinduced acute kidney injury (AKI). Acute kidney injury (AKI) is a serious disease with a high mortality rate. Rhabdomyolysis is a common clinical disorder with a broad spectrum of traumatic and non-traumatic etiologies, and approximately 10 to 50% of patients suffering from rhabdomyolysis develop some degree of AKI [1, 2]. Renal tubular damage is a pathological characteristic of AKI. Animal models of glycerol-induced AKI are widely used [3]. Glycerol injection into the muscle causes the release of myoglobin and other muscle contents into the circulation, resulting in AKI.
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