RETRACTED ARTICLE: Acute Toxicity and Gastroprotection Studies of a New Schiff Base Derived Manganese (II) Complex against HCl/Ethanol-Induced Gastric Ulcerations in Rats

Abstract

Manganese is a crucial element for health. In this study, the gastroprotective efficacy of Mn (II) complex (MDLA) against acidified ethanol (HCl/Ethanol)-induced gastric ulceration in rats was evaluated. The animals were distributed into 5 groups. Groups 1 and 2 received carboxymethylcellulose (CMC), group 3 was pretreated with omeprazole, and groups 4 and 5 were given 10 and 20 mg/kg of MDLA, respectively. After one hour, CMC and HCl/Ethanol were given to groups 2–5 whilst the animals in group 1 were ingested with CMC. After sacrifice, gastric lesions were evaluated by wall mucus, gross appearance, histology, antioxidant enzymes and immunohistochemistry. Group 2 displayed severe gastric damage with a significant reduction in wall mucus. Conversely, gastric lesions were reduced in groups 3–5 by 85.72%, 56.51% and 65.93%, respectively. The rats in groups 3–5 showed up-regulation of heat shock protein 70 (Hsp70) with down-regulation of Bcl-2-associated protein x (Bax). Pretreatment with omeprazole or MDLA led to an increase in the uptake of Periodic Acid Schiff (PAS) stain in the glandular part of the gastric tissue, raised levels of prostaglandin E2 (PGE2) and superoxide dismutase (SOD), and a reduction in malondialdehyde (MDA) concentrations. These results suggested the gastroprotective action of Mn (II) complex.

The implication of the crosstalk of Nrf2 with NOXs, and HMGB1 in ethanol-induced gastric ulcer: Potential protective effect is afforded by Raspberry Ketone

“…The areas of ulcerated lesions were determined using the image J analysis software (Image J, 1.46a, NIH, USA) and the percentages of the ulcerated areas relative to the total stomach area were calculated. The inhibition or gastroprotection percentage was determined according to the following formula [2]: …”

“…The surface of the gastric mucosa is protected by specific barrier mechanisms, such as bicarbonate secretion, mucus, prostaglandins, cell regeneration, and endogenous antioxidants. The imbalance between stressors; such as high gastric acid production, reactive oxygen species (ROS), inflammatory mediators, and Helicobacter Pylori; and protectants causes mucosal injury, and ulceration [2]. Therefore, the therapeutic strategy to protect against gastric ulcer include either intensifying gastroprotective mechanisms and/or reducing gastric-related stress factors.…”

In vivo Assessment of Antioxidant and Wound Healing Improvement of a New Schiff Base Derived Co (II) Complex in Rats

“…On the 15 th day, the animals were overdosed with xylazine and ketamine. Histological, hematological and serum biochemical parameters were assessed following standard methods1718.…”

A New Participant in the Pathogenesis of Alcoholic Gastritis: Pyroptosis

“…It has become clear that bacteria have caused gastritis in the overwhelming majority of the cases recorded since 1982 [54]. However, before that, studies have shown that alcohol causes chronic gastritis and the severity of the mucosal lesion is directly related to the duration of excess drinking [55,56]. Here, we showed that ethanol could induce pyroptosis in GES-1 cells, and this was characterized by DNA damage, the activation of caspase-1 and the release of IL-1β and IL-18.…”