Protocatechuic acid methyl ester modulates fluoride induced pulmonary toxicity in rats

We have found that protocatechuic acid methyl ester (PCAME) attenuates fluoride (F−) toxicity in lung epithelial cells (A549). However, this finding has to be confirmed with in vivo studies. Further, the effect of PCAME on F− induced pulmonary fibrosis and inflammation remains limited. Hence, the pr...

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Bibliographic Details
Published in:Food and chemical toxicology 2018-08, Vol.118, p.235-244
Main Authors: Ameeramja, Jaishabanu, Kanagaraj, Vishnu Vignesh, Perumal, Ekambaram
Format: Article
Language:English
Subjects:
Fibrosis
Fluoride
Inflammation
Lungs
Protocatechuic acid methyl ester
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Summary:We have found that protocatechuic acid methyl ester (PCAME) attenuates fluoride (F−) toxicity in lung epithelial cells (A549). However, this finding has to be confirmed with in vivo studies. Further, the effect of PCAME on F− induced pulmonary fibrosis and inflammation remains limited. Hence, the present study is aimed to determine the protective effect of PCAME against F− induced pulmonary toxicity in female albino Wistar rats. The animals were treated with sodium fluoride (NaF, 300 ppm in drinking water ad libitum) alone or in combination with PCAME (25 or 50 mg/kg bw/day by oral intubation) for 60 days and analyzed for changes in lung histology, oxidative stress, inflammation, apoptosis and fibrosis markers. PCAME supplementation prevented the F− induced changes in the above markers. Also, altered serum and bronchoalveolar lavage fluid markers and lung histoarchitecture were also restored by PCAME. F− induced modulations in oxidative stress markers, TUNEL positive cells and mRNA levels of inflammatory genes further normalized by PCAME in lung tissues. These results revealed that PCAME effectively attenuated the F− induced changes in the rat lungs by reducing cellular F− accumulation and enhancing antioxidants level. Thus PCAME can be used as a nutraceutical agent for F− toxicity. [Display omitted] •F− accumulation results in pulmonary toxicity via excess ROS generation and oxidative stress.•F− intoxication activates NFκB and TGF-β1 besides suppressing the Nrf2 signaling.•PCAME supplementation prevents the cellular F− accumulation and oxidative stress.•PCAME prevents the inflammatory and associated fibrosis progression by restoring the expression of RAGE and Nrf2.
ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2018.05.031