Metabolic profile and hepatoprotective effect of Aeschynomene elaphroxylon (Guill. & Perr.)

Abstract

Liver diseases are life-threatening and need urgent medical treatments. Conventional treatment is expensive and toxic, so the urge for nutraceutical hepatoprotective agents is crucial. This study is considered the first metabolic profile of Aeschynomene elaphroxylon (Guill. & Perr.) extracts of; flowers, leaves & bark adopting UPLC-Orbitrap HRMS analysis to determine their bioactive metabolites, and it was designed to investigate the potential hepatoprotective activity of A. elaphroxylon flowers and bark extracts against CCl4-induced hepatic fibrosis in rats. Forty-nine compounds of various classes were detected in the three extracts, with triterpenoid saponins as the major detected metabolite. Flowers and bark extracts presented similar chemical profile while leaves extract was quite different. The antioxidant activities of the flowers, leaves & bark extracts were measured by in vitro assays as Fe+3 reducing antioxidant power and Oxygen radical absorbance capacity. It revealed that flowers and bark extracts had relatively high antioxidant activity as compared to leaves extract. Based on the metabolic profile and in vitro antioxidant activity, flowers and bark ethanolic extracts were chosen for alleviation of hepatotoxicity induced by CCl4 in rats. The hepatoprotective activity was studied through measuring hepatotoxicity biomarkers in serum (ALT, AST, and Albumin). Liver tissues were examined histopathologically and their homogenates were used in determining the intracellular levels of oxidative stress biomarkers (MDA, GSH), inflammatory markers (TNF-α). Flowers and bark ethanolic extracts exerted a significant hepatoprotective effect through reduction in the activities of ALT, AST and Albumin, the tested extracts reduced oxidative stress by increasing GSH content and reducing the MDA level. Furthermore, the extracts decreased levels of pro-inflammatory TNF-α. Moreover, the present study revealed the potentiality of A. elaphroxylon in ameliorating the CCl4-induced hepatic fibrosis in rats. In this aspect, A. elaphroxylon can be used with other agents as a complementary drug.

Combination of metformin and luteolin synergistically protects carbon tetrachloride‐induced hepatotoxicity: Mechanism involves antioxidant, anti‐inflammatory, antiapoptotic, and Nrf2/HO‐1 signaling pathway

“…ROS prompts OS that can cause extreme cell damage, in this way prompting pathogenesis of numerous other remarkable diseases . The present examination affirms an expansion in the lipid peroxidation (LPO) level in CCl 4 ‐directed rodents, which is seen in their hepatic tissue (estimated as MDA), which uncovered the liver cells to oxygen‐free radicals . Moreover, these obtained outcomes are similar to the result of a past examination led on comparable topics.…”

“…37,38 The present examination affirms an expansion in the lipid peroxidation (LPO) level in CCl 4directed rodents, which is seen in their hepatic tissue (estimated as MDA), which uncovered the liver cells to oxygenfree radicals. 39,40 Moreover, these obtained outcomes are similar to the result of a past examination led on comparable topics. CCl 4 has the ability to prompt the generation of reactive oxygen-free radicals, for example, H 2 O 2 , 41,42 superoxide anions and hydroxyl radicals.…”

<p>Toxicopathological and immunological studies on different concentrations of chitosan-coated silver nanoparticles in rats</p>

“…Oxidative stress is a key mechanism inducing cytotoxicity through enhancing the production of MDA accompanied by depletion of GSH in tissues; these are considered the most important indexes of antioxidant activities 42. This may be a mechanism for the toxicity of NPs 43,44.…”

Evaluation of anti-inflammatory activity of Justicia secunda Vahl leaf extract using in vitro and in vivo inflammation models

“…This revealed that MEJSL could possess hepatoprotective effect. It has been previously shown that elevated plasma AST and ALT activities are indicators of tissue damage which are measured clinically as a diagnostic evaluation of liver function [44]. Hepatocellular damage resulting from formaldehyde-induced oxidative and inflammatory stressors could cause leakage of cytoplasmic enzymes into the plasma with concomitant increase in plasma enzyme activities.…”