Article Publish Status: FREE
Abstract Title:

Gingerol suppresses sepsis-induced acute kidney injury by modulating methylsulfonylmethane and dimethylamine production.

Abstract Source:

Sci Rep. 2018 Aug 14 ;8(1):12154. Epub 2018 Aug 14. PMID: 30108263

Abstract Author(s):

Francisco Adelvane de Paulo Rodrigues, Alan Diego da Conceição Santos, Pedro Henrique Quintela Soares de Medeiros, Mara de Moura Gondim Prata, Tailane Caína de Souza Santos, James Almada da Silva, Gerly Anne de Castro Brito, Armênio Aguiar Dos Santos, Edilberto Rocha Silveira, AldoÂngelo Moreira Lima, Alexandre Havt

Article Affiliation:

Francisco Adelvane de Paulo Rodrigues


Acute kidney injury (AKI) and metabolic dysfunction are critical complications in sepsis syndrome; however, their pathophysiological mechanisms remain poorly understood. Therefore, we evaluated whether the pharmacological properties of 6-gingerol (6G) and 10-gingerol (10G) could modulate AKI and metabolic disruption in a rat model of sepsis (faecal peritonitis). Animals from the sham and AKI groups were intraperitoneally injected with 6G or 10G (25 mg/kg). Septic AKI decreased creatinine clearance and renal antioxidant activity, but enhanced oxidative stress and the renal mRNA levels of tumour necrosis factor-α, interleukin-1β, and transforming growth factor-β. Both phenol compounds repaired kidney function through antioxidant activity related to decreased oxidative/nitrosative stress and proinflammatory cytokines. Metabolomics analysis indicated different metabolic profiles for the sham surgery group, caecal ligation and puncture model alone group, and sepsis groups treated with gingerols.H nuclear magnetic resonance analysis detected important increases in urinary creatine, allantoin, and dimethylglycine levels in septic rats. However, dimethylamine and methylsulfonylmethane metabolites were more frequently detected in septic animals treated with 6G or 10G, and were associated with increased survival of septic animals. Gingerols attenuated septic AKI by decreasing renal disturbances, oxidative stress, and inflammatory response through a mechanism possibly correlated with increased production of dimethylamine and methylsulfonylmethane.

Study Type : Animal Study

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