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

Abstract

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 β-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 β-carotene supplementation against CP-induced ALI in mice. We isolated the β-carotene from Scenedesmus obliquus microalgae n-hexane extract and identified it by HPLC and 1H-NMR analysis. Within the experiments, 40 mice were assigned into five groups randomly: Group 1 (Control): Mice received saline. Group 2 (β-carotene control): Mice were administered β-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 + β-carotene): Mice were administered β-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 β-carotene orally reduced CP-induced ALI and inflammation. β-carotene significantly decreased wet-to-dry weight ratios (W/D), down-regulated IL-17, NF-κB, and IKBKB, decreased the contents of TNF-α, COX-2, and PKC, and increased the contents of SIRT1 and PPARγ in the lung tissues. β-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 β-carotene is a promising anti-inflammatory mediator for different inflammatory-related complications.

Amentoflavone Mitigates Cyclophosphamide-Induced Pulmonary Toxicity: Involvement of -SIRT-1/Nrf2/Keap1 Axis, JAK-2/STAT-3 Signaling, and Apoptosis

“…SIRT1 belongs to the sirtuin family of proteins that have histone deacetylase activity, which plays a crucial role in cell differentiation and metabolism [36]. The affection of SIRT1 expression was suggested as a possible mechanism of CPA-induced pulmonary toxicity [37]. This may originate from the fact that SIRT1 has a unique ability to modulate the Keap1/Nrf2/ARE pathway, possibly via mitigating Keap1 expression, which, in turn, enhances the transcriptional activity of Nrf2 and augments ARE-binding ability [38].…”