The Protective Impact of Salsola imbricata Leaf Extract From Taif Against Acrylamide-Induced Hepatic Inflammation and Oxidative Damage: The Role of Antioxidants, Cytokines, and Apoptosis-Associated Genes

Abstract

Salsola imbricata is a herbal plant native to Saudi Arabia, known for its antioxidative and anti-inflammatory properties. This study explored the protective effects of an ethanolic leaf extract of Salsola imbricata against the oxidative stress and hepatic injury caused by acrylamide. Rats received intragastric administrations of 20 mg/kg of body weight of acrylamide to induce hepatic injury, or 300 mg/kg of body weight of Salsola ethanolic extract orally for 7 days before acrylamide administration. The treatments were continued for 3 weeks. Blood and liver samples were collected from all the groups, and the following biochemical parameters were tested: serum ALT (alanine aminotransferase), AST (aspartate aminotransferase), GGT (gamma glutaryl transferase), urea, albumin, total proteins, catalase, SOD (superoxide dismutase), reduced glutathione (GSH), nitric oxide (NO), and MDA (malondialdehyde). Quantitative real-time PCR (qRT-PCR) was used to examine the expression of Nrf2 (Nuclear factor-erythroid factor 2-related factor 2), HO-1 (Hemoxygenase-1), COX-2 (Cyclooxgenase-2), TGF-β1 (transforming growth factor-beta1), Bax, and Bcl2 (B-cell lymphoma 2), which are associated with oxidative stress, fibrosis, apoptosis, and anti-apoptotic effects. The annexin and survivin immunoreactivity were examined at the immunohistochemical level. Pretreatment with the Salsola ethanolic extract reduced the negative impact of acrylamide on ALT, AST, GGT, urea, albumin, and total proteins. The Salsola ethanolic extract reversed acrylamide's effects on serum and tissue antioxidants. Nrf2/HO-1 expression was downregulated, while COX-2 and TGF-β1 were upregulated in the acrylamide-administered group and normalized by the pre-administration of Salsola ethanolic extract to the acrylamide experimental group. The immunoreactivity of annexin and survivin was restored in the experimental group administered Salsola ethanolic extract plus acrylamide. In conclusion, Salsola ethanolic extract inhibits and regulates the side effects induced in the liver by acrylamide. Salsola induced its impacts by regulating inflammation, oxidative stress, and apoptosis-/anti-apoptosis-associated genes at the biochemical, molecular, and cellular levels. Salsola is recommended as oxidative stress relievers against environmental toixicity at high altitude areas.

Medicinal properties of Qatari wetland plants: A review

“…Moreover, the ethanolic leaf extracts of this species were found to regulate inflammation, oxidative stress, and antiapoptosis in hepatic inflammations, indicating potential antiinflammatory and antioxidant effects [58] . A similar investigation reported anti-inflammatory and antioxidant effects in inflammatory bowel disease [59] . However, there is a lack of sufficient evidence in the literature to indicate any potential anticancer effect of this plant species.…”

Inflammatory atherosclerotic plaque identification by SPECT/CT imaging of LFA-1 using [111In] In-DANBIRT in a novel dyslipidemic rat model

“…ZFD rat models have shown higher oxidative stress in myocytes caused by mitochondrial disruption [22]. The overaccumulation of ROS tends to conduct the mitochondria conduct autophagy and then leads to apoptosis releasing this species to the media and promoting in ammation [23,24]. ZDF rats under a HFD are known to develop hypertension with lower mitochondrial biogenesis followed by autophagy [25,26].…”

“…A colony of Apolipoprotein E knockout (ApoE KO) rats was established on the Zucker Diabetic Fatty (ZDF) background as previously detailed, utilizing the CRISPR-Cas9 system in combination with superovulation protocols [24,25] (Fig. 1).…”

Research Progress of Programmed Cell Death Induced by Acrylamide

“…It has been previously reported that AA caused apoptosis in HL7702 cells (human hepatocyte) by the disturbing cell cycle, disrupting DNA function and activating protooncogene c-jun and c-fos [87]. Studies have shown that AA induces hepatocyte apoptosis, leading to an increase of bax, TGF-β1, and COX-2 and decreases the expression of bcl-2, Nrf2, HO-1, and antioxidant [88]. AA also stimulated apoptosis in HepG2 cell, rat liver cells (e.g., BRL-3A cells and IAR20 cells), and kidney cells, and the miR-27a-5p-Btf3-ATM-p53 axis might play a vital role in the promotion of AA-induced cell apoptosis through disrupting mitochondrial structure and function [89].…”