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Year : 2019  |  Volume : 15  |  Issue : 61  |  Page : 238-243

Ameliorative effects of tannic acid on lipopolysaccharide-induced sepsis and acute lung injury in mice

1 Department of Critical Care Medicine, 521 Healthy Institutes of North Industries, Xi'an, Shaanxi, Malaysia
2 Innoscience Research Sdn Bhd, Subang Jaya, Selangor, Malaysia
3 Department of Pharmacy, Binzhou Central Hospital of Shandong, Binzhou, Shandong, Malaysia
4 Lishui Municipal Central Hospital, Lishui City, Zhejiang, China

Correspondence Address:
Tao Zhang
Lishui Municipal Central Hospital, Lishui City, Zhejiang Province 323000
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_364_18

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Background: Acute lung injury (ALI) caused by endotoxins is a severe complication causing lethal conditions. Prevention of the inflammatory response is necessary to overcome this condition. Tannic acid is a polyphenol known for its pharmacological properties such as antioxidant, antimicrobial, anti-inflammatory, anticancer, antitumor, and antimutagenic. This study aims to investigate the anti-inflammatory mechanism of tannic acid on lipopolysaccharide (LPS)-induced sepsis and ALI in mice. Materials and Methods: Male BALB/c mice were divided into five groups (n = 12) and induced with LPS (50 mg/kg body weight) and treated with tannic acid (25, 50, and 100 mg/kg) after 1 h. The bronchoalveolar lavage fluids were collected to determine the myeloperoxidase activity and levels of inflammatory cytokines (tumor necrosis factor-α, interleukin [IL]-6, and IL-1 β). Nuclear factor-kappa-β (NF-κβ) activities were examined through Western blot analysis, and hematoxylin and eosin staining was done for histopathological alterations of lung tissues. Results: Results of the study showed that tannic acid was able to prevent the infiltration of inflammatory cells and cytokines into the site of ALI which is also connected to the suppression of NF-κβ activation as shown in the Western blot analysis. The histopathological results further support these results. The safety of tannic acid was also proven on the survival of RAW264.7 cells. Conclusion: The anti-inflammatory mechanism of tannic acid on LPS-induced ALI and sepsis can be credited to the inhibition of inflammatory cytokines production mediated by NF-κβ pathway suppression. Abbreviations used: ALI: Acute lung injury; BALFs: Bronchoalveolar lavage fluids; NO: Nitric oxide; COX-2: Cyclooxygenase-2; iNOS: Inducible nitric oxide synthase; TNF-α: Tumor necrosis factor-α; IL-1β: Interleukin-1 β; IL-6: Interleukin-6.

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