Gallic acid attenuates dextran sulfate sodium-induced experimental colitis in BALB/c mice

Abstract

Gallic acid (GA) is a polyhydroxy phenolic compound that has been detected in various natural products, such as green tea, strawberries, grapes, bananas, and many other fruits. In inflammatory bowel disease, inflammation is promoted by oxidative stress. GA is a strong antioxidant; thus, we evaluated the cytoprotective and anti-inflammatory role of GA in a dextran sulfate sodium (DSS)-induced mouse colitis model. Experimental acute colitis was induced in male BALB/c mice by administering 2.5% DSS in the drinking water for 7 days. The disease activity index; colon weight/length ratio; histopathological analysis; mRNA expressions of IL-21 and IL-23; and protein expression of nuclear erythroid 2-related factor 2 (Nrf2) were compared between the control and experimental mice. The colonic content of malondialdehyde and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activity were examined as parameters of the redox state. We determined that GA significantly attenuated the disease activity index and colon shortening, and reduced the histopathological evidence of injury. GA also significantly (P<0.05) reduced the expressions of IL-21 and IL-23. Furthermore, GA activates/upregulates the expression of Nrf2 and its downstream targets, including UDP-GT and NQO1, in DSS-induced mice. The findings of this study demonstrate the protective effect of GA on experimental colitis, which is probably due to an antioxidant nature of GA.

Boldine suppresses dextran sulfate sodium‐induced mouse experimental colitis: NF‐κB and IL‐6/STAT3 as potential targets

“…MDA is the end product of lipid peroxidation, acts as a marker of oxidative stress [44]. It was well known that the level of MDA was elevated when the rodents exposed to DSS [6,9]. In consistent with the previous reports the level of MDA was elevated in DSS-induced mice (Fig.…”

“…The mice in group 3 were orally treated with boldine at the dose of 50 mg/kg body weight for 7 days. The body weights, stool consistency, and blood in the stool were monitored every day to calculate the disease activity index (DAI) [9]. The mice were sacrificed on day 8, and the colons (from the ileocecal junction to the anal verge) were removed.…”

“…During the inflammatory process, a high number of immunological cells, including activated macrophages, polymorphonuclear neutrophils, and eosinophils, infiltrate the lamina propria of the gut [7] and these cells known to produce a large amount of reactive oxygen species (ROS) [7,8]. Increased ROS leads to the oxidative damage and degrades extracellular matrix (ECM) [6,9]. Also excessive production of ROS or the impairment of antioxidant defense mechanisms may induce inflammatory and immune responses, which could directly or indirectly lead to lesion of intestinal epithelial cells and, subsequently, severe impairment in UC [10].…”

An overview on the role of dietary phenolics for the treatment of cancers

“…For example, Nrf-2, a key redox regulator, is activated by gallic acid and causes the induction of chemoresistance [131]. Similarly, a study conducted by Ashok et al 2015, also showed the ability of gallic acid to upregulate Nrf-2 activity in mice models [132]. Few recent studies have also demonstrated the ability of cinnamic acids to upregulate Nrf2.…”

Fluoxetine protects against methamphetamine-induced lung inflammation by suppressing oxidative stress through the SERT/p38 MAPK/Nrf2 pathway in rats

“…Nrf2 is a basic leucine zipper redox-sensitive transcriptional factor that serves a central role in the transcriptional regulation of antioxidant and/or detoxifying genes (19). Nuclear localization of Nrf2 activation efficiently protects cells from ROS-induced damage in vivo and in vitro by inducing the expression of numerous detoxifying enzymes and antioxidant proteins (20).…”