Evaluation of the Possible Protective Role of Nobiletin against Arsenic-Induced Liver Damage in Male Albino Rats

Abstract

Arsenic (As) is a toxic contaminant present in organic and inorganic forms in the environment. Nobiletin (NOB) is a polymethoxy flavone that has recently gained substantial consideration due to its curative impacts. The present experiment was conducted to assess the hepatoprotective efficiency of NOB on As-generated hepatotoxicity. Twenty-four adult rats were equally distributed into four groups and designated as control, As (50 mg/kg)-treated, As + NOB (50 mg/kg and 25 mg/kg, respectively), and NOB (25 mg/kg)-treated groups. After 30 days, experimental animals were decapitated, then blood and tissue samples were collected for further analysis. The group treated with As showed a significant decrease in the activity of antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione (GSH), glutathione reductase (GSR), and total antioxidant status (TAS), and a substantial increase in the accumulation of As in liver tissues, levels of total oxidant status (TOS), hydrogen peroxide (H2O2), and lipid peroxidation (TBARS). Significant increases in alanine aminotransferase (ALT), alkaline phosphatase (ALP), and aspartate aminotransferase (AST) levels were observed in As-treated rats. Moreover, nuclear factor (NF)-κB, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6, and cyclo-oxygenase (COX)-2 activity, as well as the levels of pro-apoptotic markers (Bax, Caspase-3, and Caspase-9) were increased on exposure to As. In contrast, the anti-apoptotic marker (Bcl-2) level was significantly decreased. As administration showed a significant disturbance in hepatic tissue histology. However, cotreatment of NOB with As considerably increased the antioxidant enzyme activity, with a noteworthy reduction in the deposition of As in hepatic tissues, TBARS, and H2O2 levels. NOB-administrated rats showed considerable recovery in terms of inflammation, apoptosis, and histological damage. Hence, NOB can be considered a useful curative compound due to its medicinal properties against As-prompted hepatotoxicity.

Mechanistic insight into the protective effects of fisetin against arsenic-induced reproductive toxicity in male rats

“…Whereas, the levels of TBARS and ROS were observed to be increased. The current finding is in line with our previous study, in which a decrease in activities of anti-oxidative enzymes, as well increase in lipid peroxidation and ROS were observed following the arsenic exposure 45 . However, the FIS administration escalated the activities of aforementioned antioxidative enzymes and GSH level, in addition to inhibiting the lipid peroxidation by bringing down the levels of TBARS and ROS, thereby confirming its antioxidative and anti-lipoperoxidative potential.…”

Assessment of Arsenic (As)-Induced Hepato-Nephro alterations, enzymatic inhibition and Neurobehavioral instability in Charles foster rats

“…The nding of the present study shows that exposure to three different doses of arsenic (i.e., 5mg/kg, 8mg/kg and 12mg/kg) showed saviour changes in several toxicological parameters along with signi cant reduction of body weight [15,39,46]. Compare to control group the arsenic-induced hepato-nephro organs were signi cantly (p < 0.0001) enlarged in shape and size which is also con rmed by other scientist [47]. In the exploration of haematological parameters, we nd that arsenic-induced rats had a signi cant (p < 0.0001) increase in the amount of leucocytes as well as signi cant (p < 0.0001) decrease in erythrocytes, haematocrit, mean corpuscular haemoglobin, mean corpuscular haemoglobin concentration and platelets.…”

Nobiletin from citrus peel: a promising therapeutic agent for liver disease-pharmacological characteristics, mechanisms, and potential applications

“…The hepatoprotective effect of NOB has also been reported in arsenic-induced liver injury. Ijaz et al (2023) established a liver injury model using arsenic. Their study showed that NOB decreased the release of inflammatory cytokines (TNF-α, IL-1β, and IL-6).…”