Abstract
Lauridia tetragona (L.f) R.H. Archer is routinely used in traditional medicine; however, its hepatoprotective property is yet to be scientifically proven. To this effect, the hepatoprotective activity of the polyphenolic-rich fractions (PPRFs) was investigated against acetaminophen (APAP) injured HepG2 cells. The ability of the PPRF to scavenge free radicals was tested against 2,2-diphenyl-1-picrylhydrazyl (DPPH), and [2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonicacid)] (ABTS). The ferric ion reducing power (FRAP) was also evaluated as a cell-free antioxidant assay. The hepatoprotective activity was then investigated by observing the effect of PPRFs against APAP-induced reduction in cell viability of HepG2 cells. The concentrations of alanine aminotransferase (AST), aspartate aminotransferase (ALT) and lactate dehydrogenase (LDH) released into the medium were evaluated while the underlying mechanism was further explored through western blot analysis. Thereafter, the isolated PPRFs were identified using UHPLC-QToF-MS. All six fractions of the PPRFs isolated showed significant antioxidant properties that were evident by the effective scavenging of DPPH, ABTS, and higher FRAP. The results indicated that PPRF pretreatments ameliorated APAP-induced hepatocellular injury by significantly inhibiting the leakage of AST, ALT, and LDH into the medium. The most active fractions for hepatoprotection were PPRF4 and PPRF6 with IC50 of 50.243 ± 8.03 and 154.59 ± 1.9 μg/mL, respectively. PPRFs markedly increased activities of liver superoxide dismutase, total antioxidant capacity, and liver glutathione concentration. Both PPRF4 and PPRF6 significantly increased the expression of Nrf2 and translocation. The LC-MS analysis revealed the presence of a wide variety of polyphenolics such as coumarin, ferulic acid, and caffeine among the dominant constituents. In conclusion, this study demonstrates that the isolated PPRFs have potential hepatoprotective activity that may be due to the increased expression of antioxidative genes dependent on Nrf2.
Highlights
The liver is one of the main sites for the regulation of major bodily functions such as metabolism, storage, detoxification, and secretion of drugs; any damage to the liver is often associated with distortion of these functions [1]
We evaluated the protective effect of L. tetragona against
APAP-induced cytotoxicity in HepG2 cells as a strategy to monitor the hepatoprotective activity of six fractions of the plant without high-end testing
Summary
The liver is one of the main sites for the regulation of major bodily functions such as metabolism, storage, detoxification, and secretion of drugs; any damage to the liver is often associated with distortion of these functions [1]. Hepatic injury is often caused by xenobiotics such as alcohol and chemicals have been associated with redox imbalance and oxidative stress [2]. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the antioxidant system in the liver. Recent reports suggest that oxidative stress contributes to the pathogenesis and progression of liver diseases. Reports over the past few decades implied that there is a connection between the ingestion of therapeutic doses of acetaminophen and liver injury. An increase in liver injury markers has been associated with therapeutic doses (≤4 gd−1 ) of acetaminophen [5,6,7]
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