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The Effect of Curcumin on Carbon Tetrachloride-Induced Lung Injury

Aug 2026 · Biomedicines · Vol 14, pp. 1848 · 0 citations · 41 references
Medicine

TL;DR

Findings indicate that curcumin attenuated pulmonary histopathological, biochemical, and immunohistochemical alterations associated with CCl4 exposure, accompanied by improved oxidant–antioxidant balance and reduced inflammatory, profibrotic, and apoptotic immunoreactivity.

Abstract

Background/Objectives: Carbon tetrachloride (CCl4) is a potent toxic agent that induces oxidative stress, inflammation, fibrosis, and apoptosis in various tissues, including the lungs. This study aimed to investigate the potential protective effects of curcumin against CCl4-induced lung injury in rats using histopathological, biochemical, and immunohistochemical analyses. Methods: A total of 40 male Wistar albino rats were allocated to four experimental groups: control, curcumin, CCl4, and CCl4 + Cur. Curcumin was administered orally at 200 mg/kg/day for three weeks, whereas CCl4 was administered intraperitoneally at 0.5 mL/kg as a 1:1 mixture with olive oil every other day for three weeks. Results: Histopathological examination revealed marked alveolar septal thickening, hemorrhage, vasocongestion, inflammatory cell infiltration, vacuolization, and epithelial desquamation in the CCl4 group, whereas lung tissue architecture was largely preserved in the CCl4 + Cur group. Biochemically, CCl4 exposure significantly increased the MDA levels and decreased SOD activity, while curcumin administration significantly reduced the MDA levels and increased SOD activity. Immunohistochemical H-score analysis showed significantly higher TNF-α, IL-1β, TGF-β, and caspase-3 immunoreactivity in the CCl4 group, whereas these alterations were significantly reduced following curcumin administration. Conclusions: These findings indicate that curcumin attenuated pulmonary histopathological, biochemical, and immunohistochemical alterations associated with CCl4 exposure, accompanied by improved oxidant–antioxidant balance and reduced inflammatory, profibrotic, and apoptotic immunoreactivity. However, because hepatic injury was not evaluated, the relative contributions of direct pulmonary effects and indirect liver-mediated systemic effects could not be determined.

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