Gastric Mucosal Injury In Rats Research Articles

The Role of Curcumin in Gastric Carcinoma by Modulating the Immune System and its SAR

The second most prevalent cancer in the world and the fifth most common malignant tumour is gastric carcinoma. It is thought that several factors, including genetics, epigenetics, and environmental impacts, contribute to the development of gastric cancer. One of the main pathogenic variables associated with stomach cancer risk has been identified as inflammation. There are currently few methods to treat the gastric carcinoma. Therefore, an alternative plan is urgently needed. Explaining the importance of curcumin derived from Curcuma longa Linn. in stomach cancer is the goal of this review. According to recent research, Curcumin (CUR) has a great effect against stomach mucosal injury brought on by non-steroidal anti-inflammatory medicines, gastric mucosal injury in rats, stress haemorrhage, and Helicobacter pylori infection. In this review article, we have discussed the chemistry of CUR, the role of CUR in immunomodulation, and gastric cancer. We have also highlighted the various signalling pathway of gastric cancer where CUR work. By controlling miRNAs on gastric cancer and other relevant signal pathways, CUR exhibits notable anti-inflammatory and anti-cancer properties. In future there are more research work will be done on CUR.

Antiulcer activity of the stem bark aqueous extract of Croton oligandrum (Euphorbiaceae) against Ethanol/HCl-induced gastric mucosal injury in rats

Gastric ulcer is an alteration of the lining of the stomach with destruction of mucus-producing cells. Many factors are contributing to the development of peptic ulcer such as phygiological stress, high production of acid, non-steroidal anti-inflammatory drugs (NSAIDs) and alcohol consumption. Croton oligandrum is traditionally used to treat many diseases including gastric ulcers. This study aims to investigate the cytoprotective activity of Croton oligandrum. To assess the gastroprotective potential of Croton oligandrum ulcer models were established using ethanol and indomethacin. Sucralfate was used as reference anti-ulcer drugs. Rats were treated with Croton oligandrum before induction of gastric ulceration by ethanol/HCl or HCl-ethanol-Indomethacin. The area and ulcer index appearance of ulcers were quantified, and mucus was measured. Pretreatment with Croton oligandrum showed a remarkable decrease in ulcer area when compared with control groups. Croton oligandrum (50, 100 mg/kg and 200 mg/kg of body weight) exhibited gastroprotective activity and prevented both gastric lesions induced in rats.

Herbal cake-separated moxibustion relieves aspirin induced gastric mucosal injury by activating Nrf2/ARE/HO-1 signaling in rats

To investigate whether herbal cake-separated moxibustion can activate nuclear factor erythroid 2-related factor 2 （Nrf2） / antioxidant responsive element （ARE） /hemeoxygenase-1 （HO-1） signaling pathway to repair aspirin induced gastric mucosal injury （GMI） in rats. SD rats （half male and half female） were randomly divided into blank control, model, moxibustion, inhibitor of HO-1 （inhibitor）, model+inhibitor, moxibustion + inhibitor groups, with 20 rats in each group. The GMI model was established by gavage of aspirin 150 mg/kg（1 mL/100 g）. Herbal cake-separated moxibustion was alternatively applied to bilateral "Zusanli" （ST36） and "Zhongwan" （CV12） and bilateral "Pishu" （BL20） and "Weishu" （BL21） for 30 min, once daily for 8 days. The rats in the three inhibitor groups received intraperitoneal injection of HO-1 inhibitor zinc protoporphyrin （5 mg/kg）. The rats' behavior score, emotional response score, skin hair score, diet score and stool state score were given. The GMI index was calculated according to Guth's methods. Histopathological changes of gastric mucosa were observed by H.E. staining. The activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） in the gastric mucosal tissue and serum were detected by ELISA. The levels of Nrf2/ARE/HO-1 signaling pathway-related factors Keap1, Nrf2, HO-1, CAT, GST, and NQO1 in the gastric mucosal tissue were detected by quantitative real-time PCR and Western blot, separately. Compared with the blank control group, the behavior score, emotional response score, skin hair score, diet score and stool state score, GMI index, MDA contents of gastric mucosal tissue and serum, expression le-vels of Keap1 mRNA and protein were significantly increased （P<0.01）, while the activity of gastric mucosal and serum SOD, the expression levels of Nrf2, HO-1, CAT, GST and NQO1 mRNAs and proteins were considerably decreased （P<0.01） in the model group. Compared with the model group, moxibustion obviously reversed the increase of emotional response score, skin hair score, stool state score, GMI index, MDA levels of gastric mucosal tissue and serum, and expression levels of Keap1 mRNA and protein （P<0.01, P<0.05）, and the decrease of activity of SOD of gastric mucosal and serum, and the expression levels of Nrf2, HO-1, CAT, GST and NQO1 mRNAs and proteins （P<0.01, P<0.05）. After administration of antagonist of HO-1, the effects of moxibustion were eliminated or weakened pronouncedly in reducing skin hair score, GMI index, contents of gastric mucosal and serum MDA, and expression of Keap1 mRNA and protein, and in up-regulating gastric mucosal and serum SOD, and expression of HO-1, CAT, GST and NQO1 mRNAs and proteins （P<0.01, P<0.05）. Herbal-cake separated moxibustion can improve the GMI in rats, which may be associated with its effects in reducing oxidative stress and activating Nrf2/ARE/HO-1 signaling pathway.

Protective effect of Lizhong Pill on nonsteroidal anti-inflammatory drug-induced gastric mucosal injury in rats: Possible involvement of TNF and IL-17 signaling pathways

Ethnopharmacological relevanceThe traditional Chinese medicine formula Lizhong Pill (LZP) and its herbal constituents are frequently utilized in Asian (China, Saudi Arabia, India, Japan, etc.) and some European (Russia, Sweden, UK, etc.) nations to treat various gastrointestinal ailments. Aim of the studyThis study aimed to investigate the protective impact and potential mechanism of LZP against indomethacin (IND)-induced gastric mucosal injury in rats. Material and methodsUsing a biochemical kit, we investigated the levels of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST) in rat serum, as well as pepsin in rat stomach tissue, using an IND-induced rat model of gastric mucosal injury. Various imaging tools, including HE staining, scanning electron microscopy (SEM), and transmission electron microscopy (TEM), were used to examine the gastric mucosa’s surface morphology and ultrastructure. Furthermore, molecular docking was employed to predict the binding capacity of the primary bioactive components of LZP to the critical molecular protein targets in the IL-17 and TNF signaling pathways. At the same time, immunofluorescence was used to determine the protein expressions of CASP3, VCAM1, MAPK15, MMP3, IL-17RA, and TNFR1. ResultsThe present study demonstrates that LZP (3.75 and 7.50 g/kg) significantly reduces the gastric mucosal injury index induced by IND. This effect is evidenced by the improved morphology, surface, and structure of the gastric mucosa, as determined by HE, SEM, and TEM findings. Additionally, 3.75 and 7.50 g/kg LZP intervention significantly increased SOD and CAT contents and inhibited pepsin and GST activities. Molecular docking analysis revealed that the small molecular components of LZP can bind spontaneously to crucial proteins involved in the IL-17 and TNF signaling pathways, including MAPK15, MMP3, VCAM1, and CASP3. The immunofluorescence findings proved that LZP (3.75 and 7.50 g/kg) can inhibit the protein expressions of MAPK15, MMP3, VCAM1, CASP3, IL-17RA, and TNFR1. ConclusionsOur investigation findings demonstrate that LZP can potentially ameliorate IND-induced damage to the gastric mucosa by inhibiting IL-17 and TNF signaling pathways. These results offer encouraging support for using alternative medicine to manage drug-induced gastric mucosal injury.

Repeated 28-Day Oral Toxicological Study and Gastroprotective Effects of Nigella sativa L. Oil (Shuhada) against Ethanol-Induced Gastric Mucosal Injury in Rats

Nigella sativa L. and black seeds are traditionally used for cooking and medicinal purposes in Arab and other countries. Although N. sativa seed extract has many known biological effects, the biological effects of cold-pressed N. sativa oil are poorly understood. Therefore, the objective of this study was to investigate the gastroprotective effects and subacute oral toxicity of black seed oil (BSO) in an animal model. The gastroprotective effects of oral BSO (50% and 100%; 1 mg/kg) were tested using acute experimental models of ethanol-induced gastric ulcers. Gross and histological gastric lesions, ulcerated gastric areas, ulcer index score, percentage of inhibition rate, gastric juice pH, and gastric wall mucus were all evaluated. The subacute toxicity of BSO and its thymoquinone (TQ) content were also examined. The results indicated that the administration of BSO exerted gastroprotective effects by increasing the gastric wall mucus and decreasing gastric juice acidity. In the subacute toxicity test, the animals behaved normally, and their weight and water and food intake did not show significant variations. High-performance liquid chromatography detected 7.3 mg/mL TQ in BSO. These findings suggest that BSO may be a safe therapeutic drug for preventing gastric ulcers.

Phenolic acids-rich fraction from Ficus drupacea leaves for the prevention and treatment of ethanol-induced gastric mucosal injury in rats

Bioactivity-guided fractionation of F. drupacea Thunb. extract revealed that the water fraction (FDWF) increased pH of the artificial gastric juice from 1.2 to 5.67 ± 0.015. The gastroprotective effect of FDWF against ulcer induced by ethanol was evaluated in rats. In ulcerogenic rats, increase in the gastric juice volume and ulcer lesions, and decrease in the gastric pH were evident. However, pretreatment with FDWF (100 mg/kg b.wt., p.o.) significantly inhibited lesion index, reduced gastric juice volume by 56.09% and increased gastric pH value. When given after ethanol, the same dose of FDWF led to significant healing of the gastric ulcer, with 75.60% reduction of gastric juice volume, and increase in pH value. In both prophylactic and therapeutic-treated groups, the level of superoxide dismutase and reduced glutathione in gastric homogenate were increased, while that of malondialdehyde was decreased. Also, the levels of succinate dehydrogenase and lactate dehydrogenase were increased, while that of acid phosphatase was decreased. In addition, the inflammatory markers; IL-10 and PGE2 were significantly increased. The histopathological results confirmed the above findings and indicated that the antiulcer effect of FDWF is mediated, at least in part, through antioxidant and anti-inflammatory mechanisms. Twenty-three compounds were tentatively identified in FDWF using UPLC−PDA−ESI–MS/MS and most of them were found to be phenolic acid derivatives. FDWF was standardized to contain 23.66 ± 2.62 mg/g and 8.86 ± 0.29 mg/g of quinic acid and chlorogenic acid, respectively. Accordingly, FDWF is a potential natural product that could increase the healing of gastric mucosal injury and prevents the development of ethanol-induced gastric mucosal injury in rats.

Protective Effect of Polyphenols Purified from Mallotus oblongfolius on Ethanol-Induced Gastric Mucosal Injury by Regulating Nrf2 and MAPKs Pathways.

Mallotus oblongifolius (MO), which is rich in polyphenols, is a characteristic tea resource with medicinal value. In this study, a total of 45 polyphenolic components of MO, including narirutin, isoquercitrin, rutin and digallic acid, were identified by UPLC-Q-TOF/MS analysis. In addition, the gastroprotective effect of Mallotus oblongifolius polyphenols (MOP) on ethanol-induced gastric mucosal injury in rats was investigated. The rats received anhydrous ethanol after continuous gavage of MOP or lansoprazole for one week. In addition, the macro- and micro-damage induced by ethanol in the gastric tissue was significantly reduced after MOP pretreatment for one week. Further analysis showed that MOP prevented ethanol-induced acute gastric mucosal injury by increasing the expression of antioxidant enzymes (SOD, CAT, GSH-Px) and decreasing the expression of reactive oxygen species (ROS), lipid oxidation product (MDA) and myeloperoxidase (MPO). Meanwhile, MOP inhibited the phosphorylation of p38/ERK/JNK and promoted the activation of the Nrf2 pathway. These results suggested that MOP may be a promising therapeutic target for the prevention of ethanol-induced gastric mucosal injury by improving oxidative stress, inhibiting the p38/ERK/JNK signaling pathways and activating Nrf2 expression.

Irbesartan reprofiling for the amelioration of ethanol-induced gastric mucosal injury in rats: Role of inflammation, apoptosis, and autophagy

BackgroundPronounced anti-inflammatory and anti-apoptotic features have been characterized for the angiotensin receptor blocker irbesartan. Yet, its effect on ethanol-induced gastropathy has not been studied. The present work explored the potential modulation of inflammatory, apoptotic, and autophagic events by irbesartan for the attenuation of ethanol-evoked gastric mucosal injury. MethodologyWistar rats were divided into control, control + irbesartan, ethanol, ethanol + irbesartan, and ethanol + omeprazole groups. Macroscopic examination, histopathology, immunohistochemistry, and biochemical assays were applied to examine the gastric tissues. Key findingsIrbesartan administration (50 mg/kg; by gavage) in ethanol-evoked gastropathy improved the gastric pathological manifestations (area of gastric lesion and ulcer index scores), histopathological changes, and microscopic damage scores. These beneficial effects were interceded by suppression of the HMGB1-associated inflammatory events and the linked downregulation of the nuclear NF-κBp65 protein expression. In the meantime, curtailing of the NLRP3 inflammasome by irbesartan was observed with consequent decline of the pro-inflammatory cytokine IL-1β. In tandem, upregulation of the antioxidant Nrf2 and the cytoprotective PPAR-γ were seen. Together, suppression of the pro-inflammatory cues and pro-oxidant signals attenuated the pro-apoptotic events as evidenced by Bcl-2 upregulation, Bax downregulation, and caspase 3 dampened activity. Regarding gastric autophagy signals, irbesartan diminished SQSTM-1/p62 accumulation and upregulated Beclin 1. This was associated with gastric AMPK/mTOR pathway activation evidenced by increased AMPK (Ser487) phosphorylation and lowered mTOR (Ser2448) phosphorylation. ConclusionSuppression of the inflammatory and apoptotic signals and upregulation of the pro-autophagy events may advocate the promising gastroprotective actions of irbesartan against ethanol-induced gastric injury.

Nutritional and anti-gastro ulcerative role of the gum Arabic (Acacia senegal L.) compared to a reference drug

Background: As alcohol consumption increases, ethanol impacts ulcers as a factor that causes stomach mucosal invasion, which leads to stomach ulcers. Alcohol damages the stomach through a number of processes, including increased gastric secretion, the release of pro-inflammatory cytokines, and ethanol induces a variety of pathogenic events as it is associated with the formation of stomach ulcers.Objective: The goal of this study was to see if gum Arabic as a functional food could protect albino rats against ethanol-induced stomach damage.Materials and Methods: Six groups of 30 female albino rats were formed: normal control, ulcer control, omeprazole + ethanol, and groups 4, 5, and 6, which were given GA at 7.5, 12, 25 g/ kg/ day (bw), then lab rat were given 5 mL/kg /day (bw) ethanol orally for 30 days to cause stomach mucosal damage.Results: GA suppressed gastric inflammation by lowering TNF-α and IL-6 levels while increasing IL-10 levels. GA also improved HDL, total protein, albumin, and globulin levels while lowering cholesterol, triglycerides, VLDL-C, LDL-C, and phospholipids.Conclusion: These findings demonstrate that GA plays a protective role toward gastric mucosal injury in rats induced by ethanol, which in turn reduced the inflammatory response, and significantly reduced the hemorrhagic gastric lesions and the pH of the gastric contents. Keywords: Functional food, Alcoholic, polysaccharides, soluble fiber, tumor necrosis factor alpha, oxidative stress

Preparation of deer oil powder and its effect on acute gastric mucosal injury in rats.

In this paper, deer oil was used as a raw material to prepare deer oil powder by microencapsulation technology to study the potential protective activity of deer oil powder on ethanol-induced acute gastric mucosal injury in rats. The results show that the best process for preparing deer oil powder is: the solids account for 25% of the system content, the wall material Whey Milk Protein Isolate-Maltodextrin ratio is 1:5, the Sodium Stearyl Lactate-Glycerides of Monostearate and Distearate compound emulsifier content is 0.8%, the ratio is 1:1, and the deer oil accounts for 30% of the solid content, and the spray drying inlet temperature is 180°C. Deer oil powder can reduce total stomach injury, gastric mucosal congestion area, and injury score index. Without affecting the blood lipid level, it can reduce the content of Myeloperoxidase, enhance the activity of Superoxide Dismutase and Glutathione Peroxidase, and has good antioxidant activity. Enhance the expression of defense factors Estradiol, Epidermal Growth Factor, and Somatostatin. At the same time, it reduces the levels of Interleukin-1β and Interleukin-6 pro-inflammatory cytokines in gastric tissue and enhances the expression of anti-inflammatory factors Interleukin-4 and Interleukin-10. These results indicate that the gastric protection mechanism of deer oil powder may be related to the enhancement of mucosal defense factors, inhibition of inflammation, and oxidative stress. PRACTICAL APPLICATIONS: This study screened the optimal formula for preparing microencapsulated deer oil powder and proved for the first time that deer oil powder has a strong gastroprotective effect on ethanol-induced acute gastric injury in rats. The gastric protective mechanism of deer oil powder is mainly to reduce oxidative stress, inflammatory cytokine accumulation and to increase the content of defense factors. Therefore, deer oil powder can be used as a new source of gastric treatment drugs.

Comparison of Protective Effects of Hericium erinaceus Extracts Prepared by Different Methods on Acute Gastric Mucosal Injury in Rats

Using absolute ethanol as an inducer, a rat model of acute gastric mucosal injury was constructed, and the protective effects of Hericium erinaceus crude extract prepared in several different ways on the model of acute gastric mucosal injury induced by absolute ethanol were studied. Female SD rats were randomly divided into 7 groups (n=12): Normal control group (NC), model control group (ETH), Hericium erinaceus fruit body polysaccharide intervention group(WEH1), Hericium erinaceus mycelium polysaccharide intervention group (WEH2), Hericium erinaceus water extract intervention group (WEH3), liquid fermentation water extract intervention group (WEH4) and bismuth potassium citrate granule drug group (YWZ). In each sample groups, the gavage dose (10 mL/kg) of the sample was adjusted according to the weight change, and the sample was given 167 mg/kg, bismuth potassium citrate granules (0.24 g/kg, containing 24.1 mg of bismuth) for continuous intragastric administration for 30 days. Then the normal control group and the model group were directly given distilled water, and 5 mL/kg of absolute ethanol was used to make the model. By comparing the degree of injury of gastric mucosal tissue slices, the level of inflammatory factors and the antioxidant capacity. Finally the results showed that comparing with the model group, the experimental group had significantly reduced gastric mucosal bleeding, congestion, necrosis, and pathology, and the total pathological scores were significantly different (P<0.05), the activities of superoxide dismutase (SOD) and glutathione (GSH) were significantly increased (P<0.05), the content of malondialdehyde (MDA), tumor necrosis factor-α in serum and gastric tissue (TNF-α), interleukin-6(IL-6), interleukin-1β (IL-1β) inflammatory factors levels were significantly reduced (P<0.05). So the tests have shown that several Hericium erinaceus extracts have varying degrees of protection against gastric mucosal damage in rats induced by absolute ethanol, among of them, the Hericium erinaceus mycelium polysaccharide has the best protective effect, while its mechanism of action may be similar to that of anti- oxidation is related to anti-inflammatory effects. The research results could provide a research foundation for the development and promotion of functional products of different Hericium erinaceus extracts.

Effect of Aqueous Enzymatic Extraction of Deer Oil on Its Components and Its Protective Effect on Gastric Mucosa Injury.

In this study, deer suet fat was used as a raw material to study the effects of aqueous enzymatic extraction of deer oil on its components, followed by studies into the potential protective activity, and related molecular mechanisms of deer oil on ethanol-induced acute gastric mucosal injury in rats. The results show that aqueous enzymatic extraction of deer oil not only has a high extraction yield and has a small effect on the content of active ingredients. Deer oil can reduce total stomach injury. Without affecting the blood lipid level, it can reduce the oxidative stress, which is manifested by reducing the content of myeloperoxidase (MPO) and enhancing the activity level of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). It also enhances the expression of defense factors prostaglandin (E2), epidermal growth factor (EGF), and somatostatin (SS), it inhibits apoptosis evidenced by the enhanced of Bcl-2 and decreased expression of cleavage of caspase-3 and Bax. At the same time, it reduces inflammation, which is manifested by reducing the expression of IL-1β, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) gastric tissue pro-inflammatory cytokines, and enhancing the expression of anti-inflammatory factors IL-4 and IL-10, and inhibiting the mitogen-activated protein kinase/nuclear factor kappa B (MAPK/NF-κB) signaling pathway in gastric tissue.

Effects of Three Animal Oils on Acute Gastric Mucosal Injury in Rats

Objective: To study the effects of three kinds of animal fats on gastric mucosa damage induced by ethanol in rats. Methods: Low (500 mg/kg) and high doses (850 mg/kg) of deer oil, butter and lard were given to rats by gavage for 30 days. Except for the normal group, rats in the other groups were given 1.0 mL of absolute ethanol per rat. One hour later, blood was taken from anesthesia, and gastric tissue was taken. Morphological observation, histopathological examination and the determination of acute injury indexes were performed on the gastric mucosa of rats. Detect the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in serum of rats in each group. The ELISA method was used to determine the serum levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and RT-PCR was used to detect erythropoietin (EPO) and erythropoietin receptor (EPOR) mRNA expression level. Results: Compared with the model group, the weight of rats in each administration group did not change significantly in each period. The stomach weight/body mass of the rats in the deer oil pretreatment group was extremely significantly reduced(P butter>lard. Deer oil has a significant protective effect on acute gastric mucosal injury in rats. The protective effect of butter is weak, while lard has no obvious protective effect.

Exploration of mechanism of abdominal massage to promote repair of ethanol-induced gastric mucosal injury in rats based on brain-gut axis

Exploration of mechanism of abdominal massage to promote repair of ethanol-induced gastric mucosal injury in rats based on brain-gut axis

Effects of complex extracts of traditional Chinese herbs on gastric mucosal injury in rats and potential underlying mechanism

AbstractFive complex extracts (CEs) of seven Chinese herbs (Astragalus, Poria cocos, Alpinia officinarum Hance, Radix Puerariae, Ginseng, Licorice, Hericium erinaceus) were prepared by hot water extraction and evaluated for their effect on gastric ulcer in rats. In rats with acetic acid‐induced chronic gastric ulcer, gross and microscopic appearance showed that gastric mucosal injury index and lesion inhibition rate were improved after CEs gavage for 21 days. Pretreatment with CEs for 21 days in rats with acute gastric ulcer could also improve the gastric mucosal injury by ethanol. CE1, CE4, and CE5 showed more obvious effect in two models. The cell experiments results showed that CE1, CE4, and CE5 effectively inhibited Wnt signaling activity. Thus, they could protect gastric mucosa through inhibiting Wnt signaling pathway. These results indicated that CE1, CE4, and CE5 had significant protective effects on gastric mucosal injury by inhibiting Wnt signalling pathway and could be developed into safe functional products.

Codonopsis Decoction Inhibits Aspirin-Induced Gastric Mucosal Injury in Rats by Regulating COX, COX-1, COX-2, TNF-α, IL-6 and TGF-α

Aspirin is the first non-steroidal drug used clinically in humans with a wide range of pharmacological effects [1]...

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

Background Chronic gastritis (CG) is a common digestive disease with the highest morbidity among multiple digestive diseases, which seriously lowers the life quality of patients. The pathological alternations of gastric mucosa, and its possible mechanisms have been the focus of CG-related researches. Accumulative basic and clinical evidence has confirmed that ultraviolet C (UVC) is effective in relieving superficial acute infective inflammation, skin and mucous membrane injuries, and ulcers, and promoting wound healing. Objective This study was aimed at investigating the protective effects of UVC on gastric mucosal injury in rats stimulated with physicochemical irritants like ethanol and exploring the mechanisms underlying the protection by UVC against gastric mucosal injury and CG. Methods Fifty Wistar rats were randomly divided into five groups, including Group A (normal), Group B (model), Group C (omeprazole treatment), Group D (intragastric UVC irradiation for 24 s × 2 yields), and Group E (intragastric UVC irradiation for 48 s × 2 yields). Rats in Groups B–E were made CG model by physicochemical stimulations. All rats were sacrificed one week after the 22-week experiment, and gastric tissues were harvested. Histopathological examinations were performed. The activities of superoxide dismutase and catalase as well as the contents of reduced glutathione and malondialdehyde in gastric mucosal tissues were detected. Serum interleukin-6, interleukin-1beta, tumor necrosis factor-alpha, pepsin, and gastrin were measured. Results Results showed that physiochemical irritants like ethanol could be used for easily establishing a rat CG model that shared similar pathological features with human CG. Intragastric UVC irradiation could promote the repair of gastric mucosa and improve the atrophy of gastric mucosa by inhibiting the inflammatory factors, increasing the levels of pepsin and gastrin, decreasing the expression of lipid peroxide, and enhancing the activity of superoxide dismutase and catalase and the levels of reduced glutathione. UVC irradiation for 48 s × 2 yields showed the strongest protective effect. Conclusion UVC irradiation could inhibit the inflammatory factors, activate the antioxidative system, and enhance the secretion of pepsin and gastrin, which promoted the repair of injured gastric mucosa and improved gastric mucosa atrophy.

Limb Ischemic Preconditioning or Dezocine Pre-Treatment will Reduce Acute Gastric Mucosal Injury in Rats

Limb Ischemic Preconditioning or Dezocine Pre-Treatment will Reduce Acute Gastric Mucosal Injury in Rats

Limb Ischemic Preconditioning or Dezocine Pre-Treatment will Reduce Acute Gastric Mucosal Injury in Rats

Acute gastric mucosal lesions refer to acute inflammation of the gastric mucosa [1,2], Symptoms including gastric mucosal congestion, edema, and erosion...

Russelioside B; A pregnane glycoside for treatment of gastric ulcer via modulation of heat shock protein-70 and vascular endothelial growth factor

Gastric ulcers are a very common public health problem affecting up to 10% worldwide. Russelioside B is a steroidal glycoside isolated from several Caralluma species. No study tested the ulcer healing potential of the compound. The current study aimed to assess the protective effect of russelioside B against ethanol-induced gastric mucosal injury in rats. Ulcer was induced on rats by a single intragastric dose of absolute ethanol (5 mL/kg). Rats were randomly assorted into four groups (n = 8) and given treatments (Antodine, 20 mg/kg or russelioside B, 50 mg/kg) by oral gavage 1 h before ulcer induction. Pretreatment with russelioside B (50 mg/kg) attenuated the gastric mucosal injury as proved by a decrease of ulcer index, and histological scores. It suppressed the gastric inflammation by a significant lowering the tumor necrosis factor-α and interleukin-6 levels with myeloperoxidase activity (which are also aggravating factors in the case of Covid-19 infection). In addition, administration of russelioside B halted the gastric oxidative stress via inhibition of lipid peroxides by maintaining reduced glutathione and by decreasing malondialdehyde. It was able also to restore the sharp drop in the levels of heat shock protein-70, vascular endothelial growth factor and prostaglandin E2 induced by ethanol. Additionally, it showed carbonic anhydrase inhibition activity. The gastroprotective action of russelioside B was umpired through multi mechanistic actions; suppression of gastric oxidative stress, inflammation, anti-apoptotic activities and enhanced gastric mucosal protection by up-regulation of endothelial growth factor, normalization of heat shock protein-70 and prostaglandin E2. These actions were comparable in part to some classical antiulcer drugs such as Antodine.