Combined effect of bone marrow derived mesenchymal stem cells and nitric oxide inducer on injured gastric mucosa in a rat model

Rashed, Laila Ahmed; Gharib, Doaa M.; Hussein, Rania Elsayed; Tork, Ola M.; Abusree, Azza

doi:10.1016/j.tice.2016.09.006

Cited by 11 publications

(6 citation statements)

References 26 publications

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“…Concerning the ADSCs-treated group, it showed a significant down-regulation of the Caspase-3 gene level. Our result concurs with Rashed et al ( 2016 ) who found that administration of BMMSCs to the IND-treated group considerably down-regulated Caspase-3 gene expression level. The co-treatment with ADSCs and PANTO could significantly down-regulate the Caspase-3 gene expression level due to the synergistic effect of both treatments as powerful anti-apoptotic candidates.…”

Section: Discussionsupporting

confidence: 93%

Combined effect of pantoprazole and mesenchymal stem cells on experimentally induced gastric ulcer: implication of oxidative stress, inflammation and apoptosis pathways

Sayed,

Mahmoud,

Mohawed

et al. 2024

Inflammopharmacol

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Gastric ulcer (GU) is one of the most common diseases of the upper gastrointestinal tract that affects millions of people worldwide. This study aimed to investigate the possible alleviating effect of a combined treatment of pantoprazole (PANTO) and adipose tissue-derived mesenchymal stem cells (ADSCs) in comparison with each treatment alone on the healing process of the experimentally induced GU in rats, and to uncover the involved pathways. Rats were divided into five groups: (1) Control, (2) GU, (3) PANTO, (4) ADSCs and (5) ADSCs + PANTO. Markers of oxidative stress, inflammation and apoptosis were assessed. The current data indicated that PANTO-, ADSCs- and ADSCs + PANTO-treated groups showed significant drop (p < 0.05) in serum advanced oxidation protein products (AOPPs) and advanced glycation end products (AGEPs) along with significant elevation (p < 0.05) in serum TAC versus the untreated GU group. Moreover, the treated groups (PANTO, ADSCs and ADSCs + PANTO) displayed significant down-regulation (p < 0.05) in gastric nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), intercellular adhesion molecule-1 (ICAM-1), matrix metallopeptidase 9 (MMP-9) and caspase-3 along with significant up-regulation (p < 0.05) in vascular endothelial growth factor (VEGF) and peroxisome proliferator-activated receptor gamma (PPARγ) genes expression compared to the untreated GU group. Immunohistochemical examination of gastric tissue for transforming growth factor β1 (TGF-β1), epidermal growth factor (EGF) and proliferating cell nuclear antigen (PCNA) showed moderate to mild and weak immune reactions, respectively in the PANTO-, ADSCs- and ADSCs + PANTO-treated rat. Histopathological investigation of gastric tissue revealed moderate to slight histopathological alterations and almost normal histological features of the epithelial cells, gastric mucosal layer, muscularis mucosa and submucosa in PANTO-, ADSCs- and ADSCs + PANTO-treated rats, respectively. Conclusively, the co-treatment with ADSCs and PANTO evidenced sententious physiological protection against GU by suppressing oxidative stress, inhibiting inflammation and reducing apoptosis with consequent acceleration of gastric tissue healing process.

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Section: Discussionsupporting

confidence: 93%

Combined effect of pantoprazole and mesenchymal stem cells on experimentally induced gastric ulcer: implication of oxidative stress, inflammation and apoptosis pathways

Sayed,

Mahmoud,

Mohawed

et al. 2024

Inflammopharmacol

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show abstract

“…Caspase-3 is an important member of the caspase family (cysteinyl aspartate specific proteinases), as a conjunct activating factor in apoptosis signal transduction, which directly participates in cell regulation, signal transduction and late apoptosis. Bcl-2 activates the caspase pathway, facilitates cell mitosis and inhibits apoptosis by dissolving protein structures, resulting in tumor proliferation ( 9 ). In contrast, Bax can facilitate apoptosis by forming a heterodimer with Bcl-2, essentially deterring its activity.…”

Section: Discussionmentioning

confidence: 99%

Calcium gluconate alleviates the toxic effect of hydrofluoric acid on human dermal fibroblasts through the Wnt/β‑catenin pathway

Peng

et al. 2018

Oncol Lett

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The present study was performed to determine the molecular mechanism of calcium gluconate (CG) in alleviating the toxic effect of hydrofluoric (HF) acid on human dermal fibroblasts (HDFs). HDF morphology was observed by optical microscopy and the vimentin immunofluorescence assay. Cell viability and apoptosis were evaluated by the Cell Counting Kit-8 and Annexin V/propidium iodide assays, respectively. The levels of apoptosis-associated factors, as well as Wnt2, Wnt3a and β-catenin were detected by reverse transcription-quantitative polymerase chain reaction and western blotting. Levels of matrix metalloproteinase (MMP)-1 and basic fibroblast growth factor (bFGF) were detected by ELISA and western blotting. Carboxyterminal propeptide of type I collagen (CICP) was detected by ELISA, while L-Hydroxyproline (L-HYP) was detected by colorimetry. First, the morphology of normal HDFs was observed. Cell viability was inhibited and apoptosis was increased in a dose- and time-dependent manner following treatment with HF acid [0, 2, 4, 6, 8, 10 and 20% (v/v)] for 0, 2, 4, 6, 8, 10 and 20 min. The effects were blocked by CG at different doses (50, 100 and 200 µmol/l) and time points (6, 12 and 24 h), following treatment with 8% (v/v) HF acid for 6 min. The levels of Caspase-3, B-cell lymphoma (Bcl)-2 associated X protein, Wnt2, Wnt3a and β-catenin were decreased, whereas Bcl-2 was increased by CG treatment dose-dependently, when compared with HF control. CG promoted the expression of MMP-1, bFGF and L-HYP, and inhibited CICP, when compared with HF control. Based on the present results, CG alleviated the toxic effect of HF acid on HDFs by regulating the Wnt/β-catenin signaling pathway.

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“…The increased expression of eNOS in the gastric tissue indicates a normal healing process of peptic ulcer [ 25 ] and enhancement of eNOS activity may further accelerate healing of gastric ulcers [ 26 ]. Supplement of eNOS substrate, L-arginine significantly decreased cell apoptosis in the injured gastric mucosa and improved mucosal regeneration in wild-type rats [ 27 ]. Systemic and regional inflammatory reaction is another key factor for peptic ulcer healing.…”

Section: Discussionmentioning

confidence: 99%

Exendin-4, a glucagon-like peptide-1 analogue accelerates healing of chronic gastric ulcer in diabetic rats

Chen

et al. 2017

PLoS ONE

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BackgroundDiabetes mellitus is an independent risk factor for impaired healing of peptic ulcers, and there are currently no supplementary therapeutics other than the standard antipeptic medicine to improve the ulcer healing in diabetes. This study examined the potential pleiotropic effect of a glucagon-like peptide (Glp)-1 analogue exendin (Ex)-4 on the regeneration of gastric ulcer in streptozotocin-induced diabetic rats.Methods and resultsChronic ulcer was created in rat stomach by submucosal injection of acetic acid and peri-ulcer tissues were analyzed 7 days after operation. Ulcer wound healing was impaired in diabetic rats with suppressed tissue expression of eNOS and enhanced levels of pro-inflammatory reactions. Treatment with intraperitoneal injection of Ex4 (0.5 μg/kg/d) significantly reduced the area of gastric ulcer without changing blood glucose level. Ex-4 restored the expression of pro-angiogenic factors, and attenuated the generation of regional inflammation and superoxide anions. The improvement of ulcer healing was associated with increased expression of MMP-2 and formation of granulation tissue in the peri-ulcer area.ConclusionAdministration of Ex4 may induce pro-angiogenic, anti-inflammatory and anti-oxidative reactions in the peri-ulcer tissue of diabetic rats that eventually enhances tissue granulation and closure of ulcerative wounds. Our results support the potential clinical application of Glp-1 analogues as supplementary hypoglycemic agents in the antipeptic ulcer medication in diabetes.

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Combined effect of bone marrow derived mesenchymal stem cells and nitric oxide inducer on injured gastric mucosa in a rat model

Cited by 11 publications

References 26 publications

Combined effect of pantoprazole and mesenchymal stem cells on experimentally induced gastric ulcer: implication of oxidative stress, inflammation and apoptosis pathways

Combined effect of pantoprazole and mesenchymal stem cells on experimentally induced gastric ulcer: implication of oxidative stress, inflammation and apoptosis pathways

Calcium gluconate alleviates the toxic effect of hydrofluoric acid on human dermal fibroblasts through the Wnt/β‑catenin pathway

Exendin-4, a glucagon-like peptide-1 analogue accelerates healing of chronic gastric ulcer in diabetic rats

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