Abstract
The aim of this study was to investigate the potential of postbiotics originated from Lactobacillus fermentum BGHV110 strain (HV110) to counteract acetaminophen (APAP)-induced hepatotoxicity in HepG2 cells. This strain was selected according to its autophagy inducing potential, based on previous studies reporting protective role of autophagy in APAP caused cellular damage. Cell viability was assessed using MTT and LDH assays, while autophagy was monitored by qPCR analysis of BECN1, Atg5, p62/SQSTM1, and PINK1 mRNA expression and by Western blot analysis of p62/SQSTM1 and lipidated LC3 accumulation. Our results showed that detrimental effect of APAP on cell viability was suppressed in the presence of HV110 which was linked with increased conversion of LC3 protein and p62/SQSTM1 protein degradation. Additionally, higher p62/SQSTM1 and PINK1 mRNA transcription were noticed in cells co-treated with APAP/HV110, simultaneously. In conclusion, this study suggests that HV110 enhances activation of PINK1-dependent autophagy in HepG2 cells and its eventual co-supplementation with APAP could be potentially used for alleviation of hepatotoxic side effects caused by APAP overdose.
Highlights
Acetaminophen [paracetamol, N-acetyl-p-aminophenol (APAP)] is widely used analgesic and antipyretic drug which is safe and effective at a therapeutic dose (Lee, 2004)
We initially investigated in which way HV110 affects metabolic activity of HepG2 cells
As detected decrease in metabolic activity could point on cell death, the level of lactate dehydrogenase (LDH) released in the cell culture was examined in order to determine the HV110 cytotoxicity
Summary
Acetaminophen [paracetamol, N-acetyl-p-aminophenol (APAP)] is widely used analgesic and antipyretic drug which is safe and effective at a therapeutic dose (Lee, 2004). The mechanisms of APAP-induced liver injury described to this moment include generation of reactive metabolite, N-acetyl-p-benzoquinone imine (NAPQI) and p-aminophenol (PAP) (Miyakawa et al, 2015). Given an important role of autophagy in elimination of damaged organelles, including mitochondria, it has been shown that activation of autophagy could serve as a cellular adaptive mechanism to counteract APAP-induced hepatotoxicity (Igusa et al, 2012; Ni et al, 2012). Autophagy is tightly regulated and highly inducible catabolic cellular process involved in degradation of organelles and long-living proteins. During this process double-membrane vesicles (autophagosomes) are formed and fused with lysosomes while enclosed material is degraded. Prevention of Acetaminophen Induced Hepatotoxicity by Postbiotic therapeutics capable to induce autophagy could be beneficial for liver associated pathological conditions
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