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Ellagic acid ameliorates lung damage in rats via modulating antioxidant activities, inhibitory effects on inflammatory mediators and apoptosis-inducing activities

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Abstract

Phytochemicals is considered one of the most effective and safe alternative therapy against oxidative linked lung diseases. Ellagic acid (EA), an important component of fruits, nuts, and vegetables, are partly responsible for their beneficial health effects against oxidation-related diseases. In the present study, we investigated the ameliorative effect of EA on lung damage induced by carbon tetrachloride (CCl4) in Wistar male albino rats. Thirty-six male rats (n = 36, 8-week old) were divided into 4 groups, each with 9 rats. The groups were: Control group: received standard diet; EA group: administered with EA (10 mg/kg body weight, intraperitoneal); CCl4 group: administered with CCl4 (1.5 mg/kg body weight, intraperitoneal); EA+CCl4 group: administered with EA and CCl4. . The rats were decapitated at the end of experimental period of 8 weeks and the lung tissues were examined. CCl4-induced rats showed elevation in the expressions of inflammatory proteins, nuclear factor kappa b (NF-κB), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokine, tumor necrosis factor alpha (TNF-α); and the indicator of lipid peroxidation, malondialdehyde (MDA). Intraperitoneal administration of EA significantly reduced the levels of these markers. EA administration increased the protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf-2) and enhanced the activity of glutathione (GSH) and catalase enzyme (CAT). In addition, EA administration increased the expression levels of the executioner protein of apoptosis, caspase-3, and decreasing pro-survival protein, B cell lymphoma-2 (Bcl-2). In conclusion, these results establishes the protective role of EA in the treatment of lung damage and that in the future, this may have the potential to be used as a medication for the prevention or attenuation of lung diseases.

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Abbreviations

CCl4 :

Carbon tetrachloride

EA:

Ellagic acid

EDTA:

Ethylenediaminetetraacetic acid

FUDAM:

Firat University Experimental Animals Research Institute

ip:

Intraperitoneal

MDA:

malondialdehyde

NF-κB:

Nuclear factor kappa B

PAGE:

Polyacrylamide gel electrophoresis

PMSF:

Phenylmethylsulfonyl fluoride

ROS:

Reactive oxygen species

TCA:

Trichloroacetic acid

TNF-α:

Tumor necrosis factor-α

COX-2:

Cyclooxigenase-2

SDS:

Sodium dodecyl sulfate

COPD:

Obstructive pulmonary disease

ELF:

Epithelial lining fluid

ARDS:

Acute respiratory distress syndrome

ALI:

Acute lung injury

CB:

Chronic bronchitis

ARE:

Antioxidant response element

GSH:

Glutathione

NSAIDs:

Nonsteroidal anti-inflammatory drugs

CS:

Cigarette smoke

CCl3OO•:

Trichloromethylperoxyl radical

CCl3•:

Trichloromethyl radical

TBA:

Thiobarbituric acid

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Acknowledgments

This article produced from the thesis titled “Investigation of the effect of ellagic acid on the expression of some apoptotic proteins in lung injury-induced rats” and the article was supported by Firat University Scientific Research Projects Unit (FUBAP) with FF.16.42 project number. In addition, this article presented as orally at participation in the 20th International Biotechnology Congress 10–12 October 2019, Ankara, Turkey

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Authors and Affiliations

  1. Faculty of Science, Department of Biology-Molecular Biology and Genetics Program, Firat University, Elazig, Turkey

    Abdullah Aslan

  2. Faculty of Science, Department of Biology, Firat University, Elazig, Turkey

    Yousif Taha Hussein, Ozlem Gok, Seda Beyaz & Orhan Erman

  3. Nursing Department, Halabja Technical Institute, Sulaimani Polytechnic University, Sulaimani, Iraq

    Yousif Taha Hussein

  4. Health Services Vocational High School, Department of Medical Imaging, Firat University, Elazig, Turkey

    Serpil Baspinar

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  1. Abdullah Aslan
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Aslan, A., Hussein, Y.T., Gok, O. et al. Ellagic acid ameliorates lung damage in rats via modulating antioxidant activities, inhibitory effects on inflammatory mediators and apoptosis-inducing activities. Environ Sci Pollut Res 27, 7526–7537 (2020). https://doi.org/10.1007/s11356-019-07352-8

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