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      Carvacrol attenuates acute kidney injury induced by cisplatin through suppression of ERK and PI3K/Akt activation.

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          Abstract

          We investigated the mechanisms of renoprotective effects of carvacrol, a monoterpenoid compound, against cisplatin (CP)-induced kidney injury. Male BALB/cN mice were orally administered 1, 3, and 10 mg carvacrol/kg body weight for two days, 48 h after intraperitoneal injection of CP (13 mg/kg). Four days after CP administration, renal oxidative stress was evidenced by increased expression of 4-hydroxynonenal (4-HNE), 3-nitrotyrosine (3-NT), cytochrome P450 E1 (CYP2E1), and heme oxygenase-1 (HO-1). CP treatment increased the expression of phosphorylated nuclear factor-kappaB (p-NF-κB) p65 and tumor necrosis factor-alpha (TNF-α) in kidneys, suggesting inflammatory response. CP intoxication induced apoptosis and inhibition of the cell cycle in kidneys by increasing the expression of p53 and Bax and suppressing Bcl-2 and cyclin D1 expression. Concomitant increase in p21 and proliferating cell nuclear antigen (PCNA) expression suggested enhanced DNA repair process. CP administration also resulted in activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) with concomitant induction of phosphorylated Akt and suppression of phosphatase and tensin homolog (PTEN) expression. All these changes were dose-dependently restored by carvacrol. The results of the current study suggest that carvacrol could attenuate CP-induced acute renal injury by suppressing oxidative stress, apoptosis, and inflammation through modulation of the ERK and PI3K/Akt pathways.

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          Author and article information

          Journal
          Food Chem. Toxicol.
          Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
          Elsevier BV
          1873-6351
          0278-6915
          Dec 2016
          : 98
          : Pt B
          Affiliations
          [1 ] Department of Chemistry and Biochemistry, Faculty of Medicine, University of Rijeka, Rijeka, Croatia.
          [2 ] Department of Chemistry and Biochemistry, Faculty of Medicine, University of Rijeka, Rijeka, Croatia. Electronic address: robert.domitrovic@uniri.hr.
          Article
          S0278-6915(16)30405-7
          10.1016/j.fct.2016.11.004
          27825756
          f49bda08-52c7-4a69-b89f-6de7a604eff3

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