Prevention of Rhabdomyolysis-Induced Acute Kidney Injury via Attenuation of Oxidative Injury and Inflammation by Cinnamic Acid Coated Gold Nanoparticles in Mice
Prevention of Rhabdomyolysis-Induced Acute Kidney Injury via Attenuation of Oxidative Injury and Inflammation by Cinnamic Acid Coated Gold Nanoparticles in Mice
Rehan Ahmed Siddiqui1,2*, Shabana Usman Simjee2,3, Nurul Kabir4, Muhammad Ateeq3,5, Kevin Joseph Jerome Borges6, Muhammad Raza Shah3 and Rahman M. Hafizur2
ABSTRACT
Acute kidney injury (AKI) is a life-threatening condition which may result from extensive injury to the kidney due to various causative agents. Renal insult can result from ischemia, drugs, renal obstruction, inflammation, or extensive muscle injury. The current study focused only on Rhabdomyolysis-induced AKI. We make an attempt to uncover the preventive efficacy of cinnamic acid (CA) and CA-conjugated gold nanoparticles (CA-AuNPs) against rhabdomyolysis-induced AKI induced in mice. CA (50 mg/Kg) and CA-AuNPs (30 mg/Kg) were given to the animals for four days. On the fourth day and after 24 h of water deprivation, 50% glycerol intra-muscular was administered. Blood urea and creatinine were tested. Kidney histopathology was done and damaged kidney areas were measured. Immunohistochemistry for actin and cyclooxygenase-2 (COX-2) were also carried out. Real time RT-PCR studies were performed to check mRNA expressions of nuclear factor-κB (NFκB) p50, inducible nitric oxide synthase (iNOS), kidney injury molecule-1 (Kim-1) and hemeoxygenase-1 (HO-1). CA and CA-AuNPs improved blood urea and creatinine levels when compared with the glycerol induced AKI group. The compounds kept the actin intact, decreased COX-2 protein expression, down-regulated the expressions of NFkB p50 and iNOS, and up-regulated Kim-1 and HO-1. The tested compounds (CA and CA-AuNPs) prevented the kidney from injury in the rhabdomyolysis-induced AKI animal models. However, almost complete protection is observed in CA-AuNPs treated animals at a relatively lower dose.
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