Protective Role of Casuarinin from Melaleuca leucadendra against Ethanol-Induced Gastric Ulcer in Rats

Abstract

Gastric ulcer is a major health problem. Current treatment options of gastric ulcer, including antagonists of histamine H2 receptor and inhibitors of the proton pump, do not cure gastric ulcers, but only provide temporary relief of symptoms and can be associated with severe side effects. The lack of effective and safe medications for this global health problem urges for the discovery of novel classes of compounds with potent activity and an acceptable safety profile. Ethanol-induced ulceration in rats was used to evaluate the gastroprotective activity of casuarinin, an ellagitannin isolated from Melaleuca leucadendra. Casuarinin (25, 50, and 100 mg/kg) reduced the ulcer area by 45, 78, and 99%, respectively, compared with the ulcer group. Casuarinin (100 mg/kg) increased mucin content by 1.8-fold and reduced acidity by 42%. At the same dose, it also increased the levels of reduced glutathione by 194%, catalase by 586%, and prostaglandin E2 to its normal level. In contrast, it attenuated the ethanol-increased levels of malondialdehyde by 56%, TNF-α by 58%, and caspase-3 by 87%. Histological findings demonstrated that casuarinin exhibited a protective effect against tissue alterations in response to the ethanol-induced ulcer. Casuarinin suppressed the immunoexpression of nuclear factor-kappa B, cyclooxygenase-2, and inducible nitric oxide synthase to their normal values. It also induced the expression of heat shock protein-70, reaching up to 4.9-fold in comparison with the ulcer group. The potent gastroprotective effect of casuarinin was thus attributed to its anti-inflammatory, antioxidant, and antiapoptotic effects. Our results suggest the potential application of casuarinin as an antiulcer agent from natural sources.

Chemical Constituents and Anti‐Gastric Ulcer Activity of Essential Oils of Alpinia officinarum (Zingiberaceae), Cyperus rotundus (Cyperaceae), and Their Herbal Pair

“…In contrast to COX‐1, COX‐2 is rarely expressed in normal tissues. However, after noxious stimulation, inflammatory cytokines, such as TNF‐α and IL‐6 are released, which in turn increases the expression of COX‐2 [40,41] . An increase in COX‐2 expression can aggravate gastric mucosal injury.…”

“…However, after noxious stimulation, inflammatory cytokines, such as TNF-α and IL-6 are released, which in turn increases the expression of COX-2. [40,41] An increase in COX-2 expression can aggravate gastric mucosal injury. The results of this study demonstrated that HP effectively inhibited the inflammatory cascade through the NF-кB/COX-2 signaling pathway.…”

Trimetazidine Modulates Mitochondrial Redox Status and Disrupted Glutamate Homeostasis in a Rat Model of Epilepsy

“…Hippocampal neurons were outlined, then the pathological changes in the different hippocampal regions were examined at high power (×400 magnification) in each group. The Lesion scoring system for pathological changes in different hippocampal regions was performed (Al-Sayed et al, 2020). Each animal was given a Lesion score between 0 and 3, for each of the three parameters, viz., neuronal damage, perineuronal edema, and glial cells infiltrates, where, 0 indicates no change, 1 indicates mild change (less than 15% of the examined samples), 2 indicates moderate change (16-35% of examined samples), and 3 indicates severe change (more than 35% of examined samples).…”

Protective Effect of Ultraviolet C Irradiation on the Gastric Mucosa of Rats with Chronic Gastritis Induced by Physicochemical Stimulations

“…Group A: intragastric intubation using the quartz derivation without irradiation for seven constructive days Group B: no interventions Group C: OMEP (20 mg/kg) for seven constructive days [18] Group D: intragastric UVC irradiation for 24 s × 2 yields on day 1 and intubation without irradiation on day 2 to day 7 Group E: intragastric UVC irradiation for 48 s × 2 yields on day 1 and intubation without irradiation on day 2 to day 7…”