Structure characteristics, protective effect and mechanisms of ethanol-fractional polysaccharides from Dendrobium officinale on acute ethanol-induced gastritis.

Gastritis is a common disease characterized by gastric ulcers and severe bleeding. Excessive daily alcohol consumption can cause acute gastritis, impacting individuals' quality of life. This study aims to explore the protective effects of different ethanol-fractional polysaccharides of Dendrobium officinale (EPDO) on acute alcohol-induced gastric injury in vivo. Results showed that EPDO-80, identified as a ß-glucan, exhibited significant anti-inflammatory properties in pathology. It could reduce the area of gastric mucosal injury and cell infiltration. EPDO-80 had a dose-effect relationship in reducing the levels of malondialdehyde and cyclooxygenase-2 and decreasing the levels of inflammation mediators such as tumor necrosis factor α. More extensively, EPDO-80 could inhibit the activation of the TNFR/IκB/NF-κB signaling pathway, reducing the production of TNF-α mRNA and cell apoptosis in organs. Conversely, EPDO-80 could promote changes in the gut microbiota structure. These findings suggest that EPDO-80 could have great potential in limiting oxidative stress and inflammation mediated by inhibiting the NF-κB signaling pathway, which is highly related to its ß-glucan structure and functions in gut microbiota.

Protective Effect of Mormodica balsamina Leaf Extract on the Gastric Morphology of Experimental Rats Against Ethanol Induced Gastric Ulcers / Efecto Protector de los Extractos de Hojas de Mormodica balsamina en la Morfología Gástrica de Ratas Experimentales Contra Úlceras Gástricas Inducidas por Etanol

SUMMARY: Mormodica balsamina is a valuable medicinal plant that is used to treat wounds and inflammation; its leaves are also used as an antibiotic and in the treatment of stomach pain. This study was conducted to determine the anti-ulcer activity of methanolic leaf extract of Mormodica balsamina on ethanol-induced ulcer in albino rats. A total of 32 rats were used for the study. Groups I and II served as the baseline and negative controls respectively, while groups III-VII served as the test groups. Group I was untreated, while group II received 1ml/kg body weight of the vehicle (2 % DMSO). Three test groups (III - V) received methanol extracts (75 mg, 150 mg, 300 mg/kg body weight respectively) while the other three test groups (VI - VIII) received aqueous extracts (75 mg, 150mg, 300 mg/kg body weight respectively) via oral gavage for seven days prior to ulcer induction. The rats were sacrificed, stomachs excised and ulcers scored. Histological sections were produced and examined. Findings revealed that M. balsamina extracts protected the rats' gastric epithelia from ethanol induced ulceration to varying degree with the high dose (150 and 300 mg/kg) of both extracts offering the best preservation (42 % and 50 % ulcer protective index respectively) when compared to untreated animals. Histological findings correlated with calculated ulcer indices, with treated animals having less severe gastric mucosal lesions. In conclusion, extracts of M. balsamina may possess reasonable antiulcer activities in rats against ethanol induced gastric ulcer.

Mormodica balsamina es una valiosa planta medicinal que se utiliza para tratar heridas e inflamaciones; sus hojas también se utilizan como antibiótico y en el tratamiento del dolor de estómago. Este estudio se realizó para determinar la actividad antiulcerosa del extracto metanólico de hojas de Mormodica balsamina sobre la úlcera inducida por etanol en ratas albinas. Se utilizaron un total de 32 ratas para el estudio. Los grupos I y II sirvieron como referencia y controles negativos respectivamente, mientras que los grupos III-VII sirvieron como grupos de prueba. El grupo I no se trató, mientras que el grupo II recibió 1 ml/kg de peso corporal del vehículo (2% de DMSO). Tres grupos de prueba (III - V) recibieron extractos de metanol (75 mg, 150 mg, 300 mg/ kg de peso corporal respectivamente) mientras que los otros tres grupos de prueba (VI - VIII) recibieron extractos acuosos (75 mg, 150 mg, 300 mg/kg de peso corporal respectivamente) por sonda oral durante siete días antes de la inducción de la úlcera. Se sacrificaron las ratas, se extirparon los estómagos y se puntuaron las úlceras. Se realizaron y examinaron secciones histológicas. Los resultados revelaron que los extractos de M. balsamina protegieron el epitelio gástrico de las ratas de la ulceración inducida por etanol en diversos grados, y la dosis alta (150 y 300 mg/kg) de ambos extractos ofreció la mejor conservación (42 % y 50 % de índice de protección contra úlceras, respectivamente) en comparación con los animales no tratados. Los hallazgos histológicos se correlacionaron con los índices de úlcera calculados, y los animales tratados tenían lesiones de la mucosa gástrica menos graves. En extractos de M. balsamina puede poseer actividades antiulcerosas razonables en ratas contra la úlcera gástrica inducida por etanol.

Xiaojianzhong decoction attenuates aspirin-induced gastric mucosal injury via the PI3K/AKT/mTOR/ULK1 and AMPK/ULK1 pathways.

CONTEXT: Xiaojianzhong decoction (XJZD), classically prescribed in Chinese medicine, has protective and healing effects on gastric mucosal injury. However, the exact mechanism behind this effect remains unclear. OBJECTIVE: To investigate the effect of XJZD on gastric mucosal injury and explore its underlying mechanisms. MATERIALS AND METHODS: C57BL/6 mice were randomized into six groups (n = 10): the control group receiving sterile water, the model (aspirin 300 mg/kg), the XJZD high-dose (12 g/kg), XJZD medium-dose (6 g/kg), XJZD low-dose (3 g/kg) and omeprazole (20 mg/kg) groups, by gavage daily for 14 days. The area of gastric mucosal injury, mucosal injury index and degree of histopathological damage were analysed. Gastric mucosal epithelial cell apoptosis was detected. Epithelial cell autophagy was observed. The expression levels of tight junction proteins and proteins related to apoptosis, autophagy and the pentose phosphate pathway were analysed. RESULTS: The results showed that after treatment with XJZD (12, 6 and 3 g/kg), the mucosal injury area was reduced (83.4%, 22.6% and 11.3%), the expression level of ZO-1 and occludin was up-regulated, the apoptosis rate of epithelial cells was reduced (40.8%, 25.4% and 8.7%), the expression of autophagy-related proteins LC3 and Beclin1 was decreased and the expression of p62 was increased, the PI3K/AKT/mTOR/ULK1(ser757) signalling pathway was activated, and the AMPK/ULK1(ser317) signalling pathway was inhibited. In addition, XJZD can antagonize the imbalance of redox homeostasis caused by aspirin and protect the gastric mucosa. DISCUSSION AND CONCLUSIONS: XJZD protects against aspirin-induced gastric mucosal injury, implying it to be a potential therapeutic agent.

Gastroprotective effects of Chinese Rana chensinensis skin collagen against ethanol-induced gastric ulcer in mice.

Gastric ulcer is a common gastrointestinal disease caused by excessive gastric acid secretion, which has been recognized as one of the most common causes of morbidity and mortality in the world. The skin of Rana chensinensis is rich in collagen and many previous studies have shown that it has certain bioactivity. Therefore, we extracted and purified collagen with a molecular weight less than 10000 Da from the skin of Rana chensinensis, and studied its gastric protective mechanism through the model of ethanol-induced gastric ulcer in Balb/c mice. The results showed that through macroscopic observation and significantly reduced ulcer index, it was proved that PCRCS could protect gastric mucosa and alleviate the damage of ethanol to gastric mucosa. PCRCS reduced ethanol-induced oxidative stress by boosting depleted SOD levels and dramatically lowering MDA levels, as well as significantly reducing lipid peroxidation. Additionally PCRCS (Protein Chinese Rana chesinensis Skin) additionally decreased the launch of inflammatory mediators TNF-α and IL-6 and more desirable the content material of protective elements NO and PGE2 in gastric mucosa. Based on these findings, we believe that PCRCS has potential stomach protective effects on ethanol-induced gastric ulcer, which may be achieved by inhibiting oxidative stress and stomach inflammation.

Nine geranylgeranylated derivatives isolated from the roots of Rhus chinensis Mill.

Nine undescribed geranylgeranylated derivatives (chinensens A-G), including malic acid derivative (A) and phenolic derivatives (B-E), as well as two pairs of enantiomers, [(R), (S)]-chinensens F and [(R), (S)]-chinensens G, were isolated from the roots of Rhus chinensis Mill. Their structures were elucidated by UV, IR, HRESIMS, 1D and 2D NMR spectra, as well as optical rotations. The 95% EtOH extract (95% EXT, 500 mg/kg, p. o.) of the roots of Rhus chinensis and the 95% EtOH fraction (95% FRA, 500 mg/kg, p. o.) from the microporous resin column significantly alleviated indomethacin-induced or water immersion-restraint stress-induced damage in rat gastric mucosa with inhibitory rates from 53% to 89%. The racemic mixture (chinensen G) and its enantiomers [(R), (S)]-chinensens G showed weak activities against H+,K+-ATPase (20%-24%) at a concentration of 0.1 mM, respectively.

BALB/c and C57BL/6 mouse strains influence gastric function outcomes with administration of cisplatin and dexamethasone

Abstract Our aim was to evaluate the effects of cisplatin and dexamethasone alone and combined on gastric contractility and histomorphometry of BALB/c and C57BL/6 mice. BALB/c and C57BL/6 male mice (8-week-old) were randomly separated into: Control; Cisplatin (7.5 mg/Kg); Dexamethasone (2.0 mg/Kg); and Dexamethasone plus Cisplatin (2.0 mg/Kg of dexamethasone 1-hour prior to 7.5 mg/Kg of cisplatin). Drugs were administered intraperitoneally for three days. Body weight and food intake were evaluated on 2nd day. Alternating Current Biosusceptometry technique was employed to measure gastric contractions on 3rd day. Afterward, mice were killed for gastric histomorphometric analysis. Cisplatin decreased food intake and caused bradygastria in BALB/c mice; however, the amplitude of gastric contractions decreased in both BALB/c and C57BL/6. Dexamethasone and cisplatin combined restored the gastric frequency and food intake only in BALB/c, but drug combination reduced the gastric amplitude of contractions in both strains. Dexamethasone alone increased gastric mucosa thickness in C57BL/6 and decreased muscular thickness in BALB/c. In conclusion, the mouse strains presented differences in acute effects of cisplatin and dexamethasone alone and combined on gastric function. This reinforces the importance of choosing the appropriate mouse strain for studying the acute effects of drugs on the gastrointestinal tract.

Digestion Resistance of Soybean 7S Protein and Its Implications for Reinforcing the Gastric Mucus Barrier.

Previous studies have found that soybean protein, especially soybean 7S protein (ß-conglycinin), exhibits digestion resistance, but the mechanism of digestion resistance and its implications for human health are still unclear. Here, we show that the extracted soybean 7S protein contains both oligomer globulins and amyloid aggregates, while the gastric digested soybean 7S protein only contains amyloid aggregates and thus exhibits digestion resistance. An animal experiment shows that un-digestible soybean 7S protein effectively prevents aspirin-induced acute gastric mucosa damage. The impacts of un-digestible soybean 7S protein on gastric mucus barrier properties are investigated using quartz crystal microbalance with dissipation (QCM-D), Langmuir monolayer, and multiple particle tracking (MPT). Results show that these un-digestible protein aggregates can penetrate into gastric mucus, increase the viscosity and compactness of the mucin layer, and reinforce the gastric mucus barrier properties. The findings are helpful to understand that high consumption of non-fermented soybean foods is associated with a decreased risk of gastric cancer.

Molecular Mechanism of Cinnamomum cassia against Gastric Damage and Identification of Active Compounds.

Cinnamomum cassia is a natural product found in plants that has been used as a folk remedy for inflammation. In this study, we investigated the mechanism underlying the anti-inflammatory and antioxidant properties of C. cassia extract (ECC) in lipopolysaccharide (LPS)-induced murine RAW 264.7 cells, in comparison with 4-hydroxycinnamaldehyde, a C. cassia extract component. ECC and 4-hydroxycinnamaldehyde inhibited the production of nitrite oxide in a dose-dependent manner and did not show any change in cellular toxicity when treated with the same dose as that used in the nitrite assay. Moreover, they attenuated ROS accumulation after lipopolysaccharide (LPS) stimulation. ECC and 4-hydroxycinnamaldehyde decreased the mRNA and protein expression levels of inflammatory mediators (iNOS and COX-2) and cytokines such as TNF and IL-6. We also found that ECC and 4-hydroxycinnamaldehyde mitigated the phosphorylation of ERK, JNK, and transcription factors, such as NF-κB and STAT3, suppressing NF-κB nuclear translocation in LPS-activated macrophages. In addition, administration of ECC in a Sprague Dawley rat model of acute gastric injury caused by indomethacin significantly increased the gastric mucus volume. Analysis of serum and tissue levels of inflammatory mediators revealed a significant decrease in serum PGE2 and myeloperoxidase levels and a reduction in gastric iNOS, COX-2, and p65 protein levels. Collectively, these results suggest that ECC has antioxidant and anti-inflammatory effects and is a potential candidate for curing gastritis.

Korean Red Ginseng Extract Inhibits IL-8 Expression via Nrf2 Activation in Helicobacter pylori-Infected Gastric Epithelial Cells.

Helicobacter pylori (H. pylori) causes gastric diseases by increasing reactive oxygen species (ROS) and interleukin (IL)-8 expression in gastric epithelial cells. ROS and inflammatory responses are regulated by the activation of nuclear factor erythroid-2-related factor 2 (Nrf2) and the expression of Nrf2 target genes, superoxide dismutase (SOD) and heme oxygenase-1 (HO-1). We previously demonstrated that Korean red ginseng extract (RGE) decreases H. pylori-induced increases in ROS and monocyte chemoattractant protein 1 in gastric epithelial cells. We determined whether RGE suppresses the expression of IL-8 via Nrf2 activation and the expression of SOD and HO-1 in H. pylori-infected gastric epithelial AGS cells. H. pylori-infected cells were treated with RGE with or without ML385, an Nrf2 inhibitor, or zinc protoporphyrin (ZnPP), a HO-1 inhibitor. Levels of ROS and IL-8 expression; abundance of Keap1, HO-1, and SOD; levels of total, nuclear, and phosphorylated Nrf2; indices of mitochondrial dysfunction (reduction in mitochondrial membrane potential and ATP level); and SOD activity were determined. As a result, RGE disturbed Nrf2-Keap1 interactions and increased nuclear Nrf2 levels in uninfected cells. H. pylori infection decreased the protein levels of SOD-1 and HO-1, as well as SOD activity, which was reversed by RGE treatment. RGE reduced H. pylori-induced increases in ROS and IL-8 levels as well as mitochondrial dysfunction. ML385 or ZnPP reversed the inhibitory effect of RGE on the alterations caused by H. pylori. In conclusion, RGE suppressed IL-8 expression and mitochondrial dysfunction via Nrf2 activation, induction of SOD-1 and HO-1, and reduction of ROS in H. pylori-infected cells.

The antithrombosis effect of dehydroandrographolide succinate: in vitro and in vivo studies.

CONTEXT: Dehydroandrographolide succinate (DAS) is mainly used in the clinical treatment of various infectious diseases. Its potential effects on platelet aggregation and blood coagulation systems have not been reported systematically. OBJECTIVE: To explore whether DAS exerts an antithrombotic effect and its internal mechanism. MATERIALS AND METHODS: Human blood samples and Sprague-Dawley (SD) rats divided into control, aspirin (30 mg/kg), and DAS groups (200, 400 and 600 mg/kg) were used to measure the platelet aggregation rate, coagulation function, coagulation factor activity, and contents of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1α (6-keto-PGF1α). The histopathology of the SD rat gastric mucosa was also observed. All rats were administered intragastric or intraperitoneal injections once a day for 3 consecutive days. RESULTS: Compared to control group, DAS significantly inhibited the platelet aggregation rate (ED50 = 386.9 mg/kg) by decreasing TXB2 levels (1531.95 ± 649.90 pg/mL to 511.08 ± 411.82 pg/mL) and activating antithrombin III (AT-III) (103.22 ± 16.22% to 146.46 ± 8.96%) (p < 0.05). In addition, DAS significantly enhanced the coagulation factors FV (304.12 ± 79.65% to 443.44 ± 75.04%), FVII (324.19 ± 48.03% to 790.66 ± 225.56%), FVIII (524.79 ± 115.47% to 679.92 ± 143.34%), FX (34.90 ± 7.40% to 102.76 ± 29.41%) and FXI (38.12 ± 10.33% to 65.47 ± 34.08%), increased the content of Fg (2.18 ± 0.39 to 3.61 ± 0.37 g/L), shorten the PT (10.42 ± 0.44 to 9.22 ± 0.21 s), APTT (16.43 ± 1.4 to 14.07 ± 0.75 s) and TT time (37.04 ± 2.13 to 32.68 ± 1.29 s) (p < 0.05), while the aspirin group showed no such effect on these items but showed reduced activity of FII (89.21 ± 21.72% to 61.83 ± 8.95%) and FVIII (524.79 ± 115.47% to 306.60 ± 29.96%) (p < 0.05). Histopathological changes showed aspirin-induced gastric mucosa haemorrhage and the protective effect of DAS in the gastric mucosa. CONCLUSIONS: DAS is more suitable than aspirin in thromboprophylaxis treatment, which provides a reliable theoretical and experimental basis for its clinical application.

ANKRD22 is a novel therapeutic target for gastric mucosal injury.

Ankyrin repeat domain 22 (ANKRD22) is a nuclear-encoded mitochondrial membrane protein that is highly expressed in normal gastric mucosal epithelial cells and activated macrophages. As a regulator of mitochondrial Ca2+, ANKRD22 could help repair damaged gastric mucosa by promoting the mobilization of LGR5+ gastric epithelial cells via the upregulation of Wnt/ß-catenin pathway activity in a mouse model. Furthermore, the inhibition of ANKRD22 alleviated the macrophage activation-mediated inflammatory response by reducing the phosphorylation of nuclear factor of activated T cells (NFAT). ANKRD22 plays a significant role in the repair of gastric mucosal damage and may become an ideal novel target for the treatment of gastric mucosal injury. However, there is no systematic introduction to ANKRD22 targeting. Therefore, we wrote this review to elaborate the functional mechanism of ANKRD22 in gastric mucosal injury and to analyze its potential application value in clinical therapy.

Mechanism exploration of ancient pharmaceutic processing (Paozhi) improving the gastroprotective efficacy of Aucklandiae Radix.

ETHNOPHARMACOLOGICAL RELEVANCE: Processing, also called Paozhi in Chinese, is an ancient Chinese pharmaceutic processing technique developed along with the Chinese herbal medicines (CHMs). The understanding of the mechanism of Paozhi has been investigated for several decades. Aucklandiae Radix (CAR) and its roasted processed products are all used in indigestion as a kind of CHMs. Processed Aucklandiae Radix (PAR) had a stronger effect to protect gastric mucosa than CAR, while the main compounds in CAR were reduced sharply after being processed. The underlying mechanism of this phenomenon is still unclear. AIM OF THE STUDY: This study was aimed to evaluate whether PAR have a stronger gastroprotective effect than CAR and the underlying mechanisms of such circumstance. MATERIALS AND METHODS: Ultra-fast liquid chromatography coupled with quadrupole time of flight mass spectrometry (UFLC-QTOF-MS/MS) coupled with multivariate statistical analyses was employed to explore chemical compounds which had a relatively stable content in PAR. Based on the compounds selected as the research object, network pharmacology was applied to visualize the relationships between the selected components and the gastroprotective-related targets from disease database, at the same time the possible intervention path of CAR/PAR which might be responsible for the effect of CAR/PAR on gastritis-induced rats was also built. Then, the key proteins were detected by western blotting to verify and compare the pharmacological effects of CAR/PAR. RESULTS: Through UFLC-QTOF-MS/MS and orthogonal partial least squares discriminant analysis (OPLS-DA), sixteen compounds stable in PAR were discovered, of which saussureamine C and saussureamine B were estimated as the core compounds to exert gastroprotective in PAR predicted by network pharmacology analysis. Under the guide of KEGG pathway enrichment analysis, PI3K/AKT, p38 MAPK (Mitogen-activated protein kinase) and nuclear factor-kappa B (NF-κB) signaling pathways were forecasted as the possible healing mechanisms of CAR/PAR, and that result was verified by the experiments in vivo. PAR performed a stronger ability to reduce the level of p38 MAPK and NF-κB p65 than CAR, which may partially explain the different ability of CAR/PAR against gastric mucosa damage. CONCLUSION: This study clarified that although Paozhi entailed a sharp decrease on the main compounds of CAR, there were some compounds which were not sensitive to high temperature and preserved in PAR and had a relative higher content in PAR than in CAR. PAR has stronger influence on MAPKs/NF-κB signaling pathway than CAR, which may reveal that the stronger gastroprotective effect of PAR perhaps rely on the constitutions with a higher relative abundance after Paozhi. The present research combined UFLC-QTOF-MS/MS and network pharmacology deeply investigated the impact of the roasted processing on the chemical constitutions and gastroprotective effect of CAR and offered reference for the clinical application of CAR/PAR.

Gastric acid-response chitosan/alginate/tilapia collagen peptide composite hydrogel: Protection effects on alcohol-induced gastric mucosal injury.

Long-term excessive alcohol intake can easily lead to gastritis, gastric ulcer, and gastric bleeding. In this paper, the gastric acid-responsive hydrogel of CS-NAC/alginate/tilapia collagen peptide (CS-NAC/ALG/TCP) was developed. Its structure and properties were determined. The alcohol-induced gastric mucosal injury models in mice were established to evaluate the protective effects of CS-NAC/ALG/TCP. The results showed that CS-NAC/ALG/TCP was successfully fabricated, and it showed a sustained release of TCP, strong mucoadhesion, and excellent biodegradability in vitro. In the animal experiments, CS-NAC/ALG/TCP improved the oxidative stress status of the gastric mucosa by increasing the levels of SOD, GSH, and CAT in tissues. It also down-regulated the expression of MPO, TNF-α, IL-1ß, and IL-6, and increased the production of gastric protective factors such as PGE2 and NO in mouse stomach, thereby reducing the alcohol-induced inflammation and protecting the gastric mucosal injury. Besides, CS-NAC/ALG/TCP can also increase the activities of alcohol metabolism enzymes to improve alcohol metabolism, thereby reducing alcoholic damage. In conclusion, CS-NAC/ALG/TCP is a promising candidate for the treatment of alcohol-induced gastric injury.

Protection against indomethacin-induced loss of intestinal epithelial barrier function by a quercetin oxidation metabolite present in onion peel: In vitro and in vivo studies.

Oxidative stress is directly implicated in the loss of intestinal epithelial barrier function (IEBF) induced by non-steroidal anti-inflammatory drugs (NSAIDs). Previous studies by our research team demonstrated that 2-(3,4-dihydroxybenzoyl)-2,4,6-trihydroxy-3(2H)-benzofuranone (BZF), a quercetin oxidation metabolite that naturally occurs in onion peels, exhibits an antioxidant potency notably higher than quercetin. Thus, we assessed the potential of BZF and a BZF-rich onion peel aqueous extract (OAE) to protect against the loss of IEBF in Caco-2 cell monolayers and in rats exposed to indomethacin. In vitro, pure BZF and OAE standardized in BZF (100 nM), protected against the drop in transepithelial electrical resistance by 70 - 73%. Likewise, it prevented the increase in fluorescein-isothiocyanate labelled dextran (FITC-dextran) paracellular transport by 74% and oxidative stress by 84 - 86%. In vivo, BZF, given orally at a dose 80 µg/Kg bw as OAE, totally abolished a 30-fold increase in FITC-dextran serum concentration induced by indomethacin. This effect was dose-dependent and largely conserved (85%) when OAE was given 180-min prior to indomethacin. The IEBF-protective effect of OAE was accompanied by a full prevention of the NF-ĸB activation, and the increases in interleukine-8 secretion and myeloperoxidase activity induced by indomethacin. The protection was also associated with a 21-fold increase in Nrf2, and a 7-fold and 9-fold increase in heme oxygenase-1 and NAD(P)H-quinone oxidoreductase 1, respectively. The IEBF-protecting effect of OAE involves, most likely, its dual capacity to activate Nrf2 while inhibiting NF-ĸB activation. The extremely low doses of BZF needed to promote such actions warrants extending its IEBF-protective effects to other NSAIDs.

The therapeutic effect of Huazhuojiedu decoction on precancerous lesions in a gastric cancer model via the regulation of lnc 517368.

ETHNOPHARMACOLOGICAL RELEVANCE: Huazhuojiedu decoction, a Chinese herbal preparation, has been proven to be clinically effective in treating precancerous lesions in gastric cancer (PLGC). This formula is optimized from a classic formula called "Ganluxiaodu Dan." Although some experiments have shown that Huazhuojiedu decoction is effective against PLGC, the mechanism remains unclear. AIM OF THE STUDY: To investigate the treatment of PLGC with Huazhuojiedu decoction from the perspective of lncRNA in vitro and in vivo. MATERIALS AND METHODS: A PLGC rat model was prepared and randomly divided into a Huazhuojiedu decoction group (HG), a vitacoenzyme group (VG), a model group (MG), and a normal group (CG). Each group was given a corresponding concentration of medicine and distilled water for 10 weeks. The pathological changes in the gastric mucosa were observed by hematoxylin-eosin staining (HE). High-throughput sequencing was performed to detect the differentially expressed lncRNAs in the HG, MG, and CG. Quantitative real-time reverse transcription-polymerase chain reaction (RT-qPCR) was used to verify differentially expressed lncRNAs, and rat-human homology information was obtained from the University of California, Santa Cruz (UCSC) Genome Database. Human gastric mucosal epithelial cells (GES-1) were used to prepare precancerous lesions of gastric cancer cells (MC). A Huazhuojiedu decoction drug-containing serum was prepared to treat the MC cells. The effects of the Huazhuojiedu decoction and the lncRNA ENST00000517368 (lnc 517368) knockdown or overexpression on PLGC cell proliferation and apoptosis were evaluated in vitro using CCK-8, flow cytometry, and RT-qPCR. RESULTS: The HE results showed that gastric mucosal pathology was significantly improved in the HG. High-throughput sequencing results showed that compared with the CG, 91 lncRNAs upregulated in the MG were restored and downregulated in the HG (P < 0.05), and 115 lncRNAs downregulated in the MG were restored and upregulated in the HG (P < 0.05). The results of RT-qPCR were consistent with the sequencing results. The differentially expressed genomic rat lncRNA ENSRNOT00000079699 is homologous to human lnc 517368. In cell experiments, high expression of lnc 517368 promoted proliferation and reduced apoptosis in PLGC cells, while the Huazhuojiedu decoction reduced the expression of lnc 517368 and improved cell morphology. CONCLUSIONS: Huazhuojiedu decoction inhibited cell proliferation and promoted apoptosis in PLGC cells, and its effect may be partially dependent on the downregulation of lnc 517368.

Mechanisms of Dendrobium officinale polysaccharides in repairing gastric mucosal injuries based on mitogen-activated protein kinases (MAPK) signaling pathway.

The present study aimed to investigate the protective effects and molecular mechanisms of Dendrobium officinale polysaccharides on gastric mucosal injuries. Following one week of continuous intragastric administration, a gastric mucosal injury model was established using intragastric administration of anhydrous ethanol. The area of gastric ulcer was measured, the contents of interleukin- 6 (IL-6), epidermal growth factor receptor (EGFR), and thyroid transcription factor 1 (TFF-1) in serum were detected by enzyme linked immunosorbent assay (ELISA), and the expressions of EGFR, TFF-1, IL-6, Raf-2, MAP kinase kinase 1 (MEK1), MEK2, and ERK1 in the gastric tissue were determined utilizing qPCR, Western blotting and immunohistochemistry. Simultaneously, Dendrobium officinale polysaccharides and anhydrous ethanol were added to the gastric mucosal cells (GES1) cultured in vitro, and the protective effects of Dendrobium officinale polysaccharides on cell viability was detected using Cell Counting Kit (CCK)-8. The addition of Dendrobium officinale polysaccharides markedly improved the gastric epithelial defect, inflammatory cell infiltration, and redness and swelling stemmed from gastric mucosal injuries and greatly reduced the area of gastric ulcer. The inhibition rates of gastric ulcer were 48.12 ± 2.98, 42.95 ± 1.52, and 27.96 ± 2.05% in the high, medium, and low concentration Dendrobium officinale polysaccharide groups, respectively. Dendrobium officinale polysaccharides could increase the expressions of EGFR and TFF-1 and decrease the expressions of IL-6, Raf-2, MEK1, MEK2, and ERK1. Dendrobium officinale polysaccharides could reduce the level of inflammatory factors and protect gastric mucosa by inhibiting the expression of MAPK pathway genes and proteins.