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Updated: Aug 28, 2026

Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube
Published on: April 28, 2020
The Effect of Curcumin on Carbon Tetrachloride-Induced Lung Injury
Şahinaz Atalay1, Mete Keçeci1, Meryem Akpolat Ferah1
1Department of Histology and Embryology, Faculty of Medicine, Zonguldak Bülent Ecevit University, 67630 Zonguldak, Türkiye.
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.
