The potential protective effect of Commelina nudiflora L. against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats, mediated by suppression of oxidative stress and inflammation

Abstract

BackgroundThis study aims to assess the hepatoprotective potential of Commelina nudiflora against CCl4-induced hepatic injury in rats.MethodAntioxidant activities were determined. Phytochemical analysis was performed by gas chromatography mass spectrometry (GCMS). In the in vivo study, Sprague Dawley rats were pretreated with C. nudiflora (150, 300, and 450 mg kg body weight (b.wt.)) once daily for 14 days followed by two doses of CCl4 (1 ml/kg b.wt.). After 2 weeks, the rats were sacrificed and hepatoprotective analysis was performed.ResultsIn vitro studies have shown that the extract possessed strong antioxidant activity and has ability to scavenge 2,2-diphenyl-2-picrylhydrazyl-free radicals effectively. GCMS analysis of the C. nudiflora extract revealed the presence of various bioactive compounds. Administration of C. nudiflora significantly reduced the impact of CCl4 toxicity on serum markers of liver damage, serum aspartate transaminase (AST), and alanine transaminase (ALT). C. nudiflora also increased antioxidant levels of hepatic glutathione (GSH) and antioxidant enzymes and ameliorated the elevated hepatic formation of malondialdehyde (MDA) induced by CCl4 in rats. Histopathological examination indicated that C. nudiflora protect the liver from the toxic effect of CCl4 and healed lesions such as necrosis, fatty degeneration, and hepatocyte injury as irregular lamellar organization and dilations in the endoplasmic reticulum. The immunohistochemical studies revealed that pretreatment of C. nudiflora decreased the formation of 4-hydroxy-2-nonenal (HNE)-modified protein adducts and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Furthermore, overexpression of the proinflammatory cytokines TNF-α, IL-6, and prostaglandin E2 is also reduced.ConclusionThese findings exhibited the potential prospect of C. nudiflora as functional ingredients to prevent ROS-related liver damage.

R. verniciflua and E. ulmoides Extract (ILF-RE) Protects against Chronic CCl4-Induced Liver Damage by Enhancing Antioxidation

“…In liver injury, CCl 4 is biotransformed by the catalytic activity of the liver cytochrome P450 in the ER to generate free radicals, primarily trichloromethyl free radicals ( • CCl 3 or CCl 3 OO • ) as the hepatotoxic metabolites of CCl 4 . These have the potential to bind to various proteins or lipids and initiate lipid peroxidation [ 32 , 33 ], resulting in a loss of cell membrane integrity and liver injury [ 32 ], whereas ILF-RE significantly increased the activity of antioxidant enzymes GPx, SOD, and catalase against the hepatotoxic metabolite-associated ROS and damage, thus decreasing serum AST and ALT levels ( Figure 3 ). Since these enzymes serve as the first line of defense to counteract free radical-induced oxidative stress [ 34 ], endogenous anti-oxidative enzyme activity is strongly considered one of the primary mechanisms underlying ILF-RE-induced protective effects.…”

The Great Healing Potential Hidden in Plant Preparations of Antioxidant Properties: A Return to Nature?

“…Additionally, plant origin substances were proved to decrease mouse mortality resulting from the acute CCl 4 toxicity [ 78 ] as well as from Concanavalin A exposure [ 79 ]. Furthermore, several studies included the influence of plant materials alone, and generally, no harmful effects were observed [ 14 , 54 , 74 , 75 , 78 , 80 , 81 ].…”

“…In many studies, the protective effects of plant extracts and constituents showed a direct dependency on the used dose [ 15 , 29 , 31 , 56 , 80 , 107 , 117 ].…”

Lactobacillus fermentumHFY06 reduced CCl4-induced hepatic damage in Kunming mice

“…It plays important roles in maintaining human health via oxidation, glycogen storage, detoxication, immunity, and protein secretion. [1][2][3] It is also susceptible to a range of stimuli, including viruses, toxins, drugs, alcohol and trauma, which can eventually lead to acute or chronic liver damage. 4,5 For example, excessive use of carbon tetrachloride (CCl 4 ) can cause severe liver damage, which may lead to liver failure and even death.…”