Gastroprotective Effect of Polypeptide-K Isolated from Momordica charantia’s Seeds on Multiple Experimental Gastric Ulcer Models in Rats

Peptic ulcer disease is a multifactorial disorder and is the most significant public health concern nowadays. Previous study showed that essential oil extracted from Momordica charantia’s seed exhibited gastroprotective effect. However, the evidence for the gastroprotective effect of its active compound, polypeptide K (PPK), remains unclear. This study aimed to examine the preventive effect of PPK against different experimental gastric lesions models in rats. The possible gastroprotective effect of PPK was assessed in hydrochloride ethanol- and indomethacin-induced gastric ulcer models in Sprague Dawley rats and was further evaluated macroscopically and microscopically. Pyloric ligation experiments were used to investigate gastric secretion. Oral administration of PPK at all concentrations (10, 25, and 50 mg/kg) showed significant p < 0.05 reduction in total area of lesion in both hydrochloride ethanol- and indomethacin-induced gastric ulcer models. The highest inhibition rate was seen in PPK dose of 50 mg/kg with 64.9% and 72.2% on hydrochloride ethanol and indomethacin models, respectively. Microscopically, PPK preserved the normal architectures of the gastric tissues from being damaged by hydrochloride ethanol and indomethacin. Further, in the pyloric ligation studies, PPK significantly p < 0.05 decreased the ulcer area where the highest protection was exhibited by 50 mg/kg with 70% inhibition rate. Moreover, all concentrations of PPK also significantly p < 0.05 enhanced the gastric wall mucus secretion. Collectively, this study demonstrated the gastroprotective effect of PPK on hydrochloride ethanol- and indomethacin-induced gastric ulcer models. The possible mechanism might be associated with enhanced mucus secretion and thus lowering the total acidity.

Gastroprotective Effect of Conocarpus Erectus Plus Omega-3 on Experimentally Induced Ulcer in Rats

There has been a dearth of research on the gastroprotective effect of Conocarpus erectus in the literature so the current study was designed to estimate the ability of Conocarpus erectus (C. erectus) leaves extract alone and in combination with omega-3 regarding gastroprotective effects. A total of 30 male rats were divided into five groups (n = 6). All animals induced gastric ulcer by 80 mg/kg of naproxen orally twice a day for three consecutive days. At the same time, the animals treated orally with 175 mg/kg omega-3, 250 mg/kg C. erectus, 80 mg omega-3 + 150 mg C. erectus, 10 mg/kg of lansoprazole, and 2 ml/kg of DMSO were named T1, T2, T3, T4, and TC, respectively. The obtained results of the present study indicated the presence of flavonoids, saponin, and tannin as active ingredients in C. erectus leaves extract. Consequently, C. erectus seemed to have the potential of chelating metals in a concentration-dependent manner. Gross and histopathology findings showed the highly protective capability of C. erectus and omega-3 against ulcerative lesion, compared to the time each was used alone. The outcomes of the current study indicated that using C. erectus alone or plus omega-3 can protect the gastric mucosa from the ulceration induced by naproxen, and the chelating properties of C. erectus.

Gastroprotective Effects of the Aqueous Extract from Taraxacum officinale in Rats Using Ultrasound, Histology, and Biochemical Analysis

Taraxacum officinale F.H. Wigg. belonging to the family Asteraceae is an edible medicinal plant distributed worldwide. This study aimed to determine the gastroprotective effects of aqueous extract of T. officinale (AETo) in rats using ultrasound, histological, and biochemical analyses. In this study, gastric ulceration was induced by ethanol or piroxicam. Rats were then treated with AETo (3, 30, or 300 mg/kg). The area and histological appearance of gastric ulcers were quantified, and histochemical analysis was performed. The activity of AETo on inflammatory and oxidative stress markers was assessed in the ulcerated tissue. In addition, we investigated the thickness of the gastric wall using the ultrasound technique. Moreover, chemical analyses of AETo were performed. In rats with ethanol- or piroxicam-induced ulcers, AETo reduced the ulceration area, elevated mucin level, and the gastroprotective effect was confirmed by histological analysis. The gastroprotective effect was accompanied by increased activities of SOD, CAT, and GST, as well as an increase in GSH level and reduction in MPO activity. Furthermore, AETo reduced the thickness of the gastric wall in rats. Phytochemical analysis of AETo indicated phenolic acids and flavonoids as the main active compounds. In conclusion, the gastroprotective effect of AETo involves reduction in oxidative stress and inflammatory injury and increase in mucin content. This study advances in the elucidation of mechanisms of gastric protection of T. officinale, contributes to the prospection of new molecules gastroprotective, and proposes the ultrasonographic analyses as a new gastroprotective assessment tool in preclinical studies.

The Gastroprotective Effect of Naringenin against Ethanol-Induced Gastric Ulcers in Mice through Inhibiting Oxidative and Inflammatory Responses

Naringenin is a major flavanone found in grapes, tangelos, blood oranges, lemons, pummelo, and tangerines. It is known to have anti-inflammatory, antioxidant, anticancer, antimutagenic, antifibrogenic, and antiatherogenic pharmacological properties. This study aims to investigate the anti-inflammatory effects of naringenin in ethanol-induced gastric damage in vivo and ethanol-stimulated KATO III cells in vitro. Our results showed that pretreatment with naringenin significantly protected mice from ethanol-induced hemorrhagic damage, epithelial cell loss, and edema with leucocytes. It reduced gastric ulcers (GU) by suppressing ethanol-induced nuclear factor-κB (NF-κB) activity and decreasing the levels of nitric oxide (NO), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-8 (IL-8), and myeloperoxidase (MPO). In addition, pretreatment with naringenin might inhibit the secretion of TNF-α, IL-6, and IL-8, as well as the proteins cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) via the suppression of NF-κB and mitogen-activated protein kinase (MAPK) signaling in ethanol-stimulated stomach epithelial KATO III cells. Together, the results of this study highlight the gastroprotective effect of naringenin in GU of mice by inhibiting gastric secretion and acidity, reducing inflammation and oxidative stress, suppressing NF-κB activity, and restoring the histological architecture. These findings suggested that naringenin has therapeutic potential in the alleviation of ethanol-induced GU.

Gastroprotective Effect of Enteral Nutrition Formula in Mice Injected Subcutaneously with Indomethacin

We have previously shown that two enteral nutrition formulas suppressed gastric lesions induced by the oral administration of indomethacin (IND) in mice. However, the mechanism of their protective effect is unknown. In this study, the effect of the two enteral nutrition formulas on gastric lesions induced by subcutaneous IND injection was investigated, with the objective of exploring the possibility that they may interact directly with IND in the gastrointestinal tract. Ten-week-old, male, ICR mice were fasted, then orally given either purified water, Mermed® One, or 2-fold diluted Terumeal® 2.0α as enteral nutrition formula (25 mL/kg). IND was injected subcutaneously at 20 mg/kg after 30 min, and the stomach was removed 6 h later and fixed in formalin. The number and area of lesions in the stomachs of mice given enteral nutrition formula was reduced to 56–89% and 34–61%, respectively, compared with the mice given purified water. The time courses of plasma IND concentrations were comparable among the three groups. These results suggested that the effect of these enteral nutrition formulas on gastric lesions did not originate from their direct interaction with IND in the gastrointestinal tract or their effect on the disposition of IND.

Gamma (γ)-mangostin attenuated gastric ulcers induced by absolute alcohol in rats: Histological, immunohistochemical and biochemical investigation

Garcinia mangostana L. (Clusiaceae) principally contains gamma (γ)-mangostin, a xanthone that exhibits a wide spectrum of bioactivities. The current study was aimed to establish the gastroprotective effect of this compound in ethanol-induced gastric mucosal injuries in rats. Experimental Sprague Dawley (SD) rats (n = 30) were arbitrarily alienated into 5 groups (n = 6): negative control (10% Tween 20), ulcer control (10% Tween 20 + 5ml/kg absolute alcohol), reference control (5ml/kg absolute alcohol + 20mg/kg omeprazole), and two experimental groups (5ml/kg absolute alcohol + 10mg/kg γ-mangostin and 5ml/kg absolute alcohol + 20mg/kg γ-mangostin). After successful oral feeding, all rats were anesthetized and sacrificed. Gastro-histology highlighted severe injuries to the gastric mucosa with decrease in gastric mucosal content and gastric juice pH in ulcer control group. γ-mangostin (10 mg/kg & 20 mg/kg) showed strong gastroprotective effect by enhancing gastric mucosal content and gastric juice pH compared to the ulcer group, comparable to the omeprazole. Immuno-histochemical analysis revealed that γ-mangostin found to upregulate mucosal Hsp70 protein, and down-regulate Bax proteins. The biochemical analysis of mucosal tissue homogenate showed significant antioxidant activity with increase in SOD and CAT activities, whereas MDA was significantly decreased at p < 0.001. The histological, immuno-histochemical and biochemical analysis evidenced gastroprotective effects of γ-mangostin that are attributed to its potential to inhibit alcohol induced oxidative stress. Specifically, γ-mangostin improved histology of mucosal content and enhanced anti-oxidative enzymes (SOD & CAT) with decreasing lipid peroxidation (MDA). Furthermore dose dependent administration of γ-mangostin down-regulated expression of Bax protein and up-regulated HSP70.