Boswellic Acid Synergizes With Low-Level Ionizing Radiation to Modulate Bisphenol Induced-Lung Toxicity in Rats by Inhibiting JNK/ERK/c-Fos Pathway

Abstract

Bisphenol A (BPA) is a low molecular weight chemical compound that has a deleterious effect on the endocrine system. It was used in plastics manufacturing with injurious effects on different body systems. Occupational exposure to low-level ionizing radiation (<1 Gy) is shown to attenuate an established inflammatory process and therefore enhance cell protection. Therefore, the objective of this study was to investigate the protective effect of boswellic acid (BA) accompanied by whole-body low-dose gamma radiation (γ-R) against BPA-induced lung toxicity in male albino rats. BPA intoxication induced with 500 mg/kg BW. Rats received 50 mg BA/kg BW by gastric gavage concomitant with 0.5 Gy γ-R over 4 weeks. The immunoblotting and biochemical results revealed that BA and/or γ-R inhibited BPA-induced lung toxicity by reducing oxidative damage biomolecules; (MDA and NADPH oxidase gene expression), inflammatory indices (MPO, TNF-α, IL-6, and gene expression of CXCR-4). Moreover, BA and or/γ-R ameliorated the lung inflammation via regulation of the JNK/ERK/c-Fos and Nrf2/ HO-1 signaling pathways. Interestingly, our data demonstrated that BA in synergistic interaction with γ-R is efficacious control against BPA-induced lung injury via anti-oxidant mediated anti-inflammatory activities.

Bisphenol-A/Radiation mediated inflammatory response activates EGFR/KRAS/ERK1/2 signaling pathway leads to lung carcinogenesis incidence

“…Lung cells include estrogen receptors, which stimulate their growth. 23 According to the previous studies, 7 , 10 which found that BPA-induced lung injury in rats, the present study revealed that exposure to BPA along with ionizing radiation interactions influences cellular responses and induces small cell lung cancer (SCLC) in female rats confirmed by bio and histology analysis. The estrogen receptor GPER mediated this effect through which the BPA/IR prompted activation signals GPCR/EGFR/KRAS/ERK1/2 stimulates upregulation of MMP-2 and MMP-9.…”

“…BPA also stimulates MAPK/ERK and p-JNK signaling pathway members' transcription and translocation. 7 Moreover, living organisms are exposed to ionizing radiation (IR) in everyday life, which is a phenomenon that has the potential to cause harmful human health impacts. Staff in the sectors of radiation and nuclear-powered engineering, patients having diagnostic procedures and/or treatment activities, and medical workers accidentally exposed to some degree of radiation are among the people and humanities who are exposed to IR from natural and manufactured sources.…”

“…However, there is little evidence to support this idea, and the underlying processes remain unknown. Therefore, according to the previous studies, 7 , 10 the current study aimed to look into the effects of toxic pollutants like BPA and ionizing radiation stressors on rat lung health. Also, a proposed mechanism for their deleterious effect on the lung tissue was revealed.…”

New Insights into How Melatonin Ameliorates Bisphenol A-Induced Colon Damage: Inhibition of NADPH Oxidase

“…Scientific research clarified the distribution of NOX homologs in the colon and confirmed their contribution to the pathological processes of intestinal diseases . It is reported that the transcript levels of the NOX gene in rat lungs are overexpressed due to BPA exposure . Xia et al reported that BPA promotes ROS formation in human colon cancer cells in a NOX-dependent manner .…”

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“…It decreases the oxidative damage of the bio-molecules (NADPH and MDA) and inflammatory variables (IL-6, TNF-α, and MPO). It also inhibits lung inflammation by preventing JNK/ERK/cFos pathway 28 .…”