Natural β-carotene prevents acute lung injury induced by cyclophosphamide in mice

IL-17 is associated with varied inflammatory and immune-related diseases. However, the biological function of IL-17 and its expression in acute lung damage are not entirely known. Thanks to the powerful antioxidant properties of beta-carotene, we presumed that it would show a potent protecting effect against cyclophosphamide (CP) -induced acute lung injury (ALI) in mice. We studied the mechanisms underlying the effect of beta-carotene supplementation against CP-induced ALI in mice. We isolated the beta-carotene from Scenedesmus obliquus microalgae n-hexane extract and identified it by HPLC and H-1-NMR analysis. Within the experiments, 40 mice were assigned into five groups randomly: Group 1 (Control): Mice received saline. Group 2 (beta-carotene control): Mice were administered beta-carotene (40 mg/kg; orally) once daily for 10 sequent days without CP injection. Group 3 (CP): One i.p injection of 200 (mg/kg) of CP was given to mice. Group 4 and 5 (CP + beta-carotene): Mice were administered beta-carotene (20 and 40 mg/kg; orally) once a day for ten days following the CP injection. Lung samples were collected for lab analysis, after scarifying the animals at the experiment end. Administration of beta-carotene orally reduced CP-induced ALI and inflammation. beta-carotene significantly decreased wet-to-dry weight ratios (W/D), down-regulated IL-17, NF-kappa B, and IKBKB, decreased the contents of TNF-alpha, COX-2, and PKC, and increased the contents of SIRT1 and PPAR gamma in the lung tissues. beta-carotene ameliorated the histopathological changes induced by CP and reduced the scoring number of inflammatory cell infiltration and emphysema when compared to CP. Consequently, we conclude natural beta-carotene is a promising anti-inflammatory mediator for different inflammatory-related complications.