Camphor alleviates renal fibrosis by suppressing oxidative stress and inflammation, up-regulating SIRT1 and down-regulating NF-κB and TGF-β.

Renal fibrosis is the main pathological change observed in the progression of chronic kidney disease. This study aimed to investigate the effects of camphor (a type of monoterpene) on the biochemical, molecular, histopathological, and functional alterations associated with thioacetamide (TA)-induced kidney fibrosis in adult male Wistar rats. Animals were divided into four groups: Control, Camphor, TA, and TA + Camphor. Intraperitoneal administration of camphor (10 mg/kg, daily) and TA (200 mg/kg, twice a week) was conducted for a duration of 4 weeks. Camphor reduced malondialdehyde and nitric oxide levels in the kidneys of rats treated with TA and increased glutathione content and superoxide dismutase activity. It decreased the expression of proinflammatory cytokines, nuclear factor kappa-B (NF-κB), and transforming growth factor-beta (TGF-β). Camphor also stimulated sirtuin 1 (SIRT1) expression. This monoterpene inhibited collagen expression and deposition in the kidneys and reduced histopathological damage. It also lowered the levels of creatinine and serum blood urea nitrogen and decreased the expression of kidney injury molecule-1. We concluded that camphor alleviates TA-induced renal fibrosis by reducing oxidative stress and inflammation. Its renoprotective effects are achieved through the upregulation of SIRT1 and the downregulation of NF-κB and TGF-β.