scholarly journals Brassica oleracea var. capitata L. Alleviates Indomethacin-Induced Acute Gastric Injury by Enhancing Anti-Inflammatory and Antioxidant Activity

Processes ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 372
Author(s):  
Seong Hwan Ryou ◽  
Il Je Cho ◽  
Beom-Rak Choi ◽  
Moon Bong Kim ◽  
Young Sam Kwon ◽  
...  
Keyword(s):  
Brassica Oleracea ◽  
Inflammatory Responses ◽  
Nuclear Factor Κb ◽  
Gastric Injury ◽  
Gastric Tissue ◽  
Sprague Dawley ◽  
White Cabbage ◽  
Histological Score ◽  
Vitamin U ◽  
Ulcerative Lesions

Brassica oleracea var. capitata L. (white cabbage) is a valuable vegetable with diverse nutraceutical benefit. Present study aimed to investigate the preventive effects of B. oleracea extract (BOE) standardized by vitamin U on indomethacin (IND)-induced acute gastric injury in Sprague-Dawley rats. Pre-administration of three different doses of BOE (12.5–50 mg/kg) for 14 days significantly decreased visible ulcerative lesions in the gastric tissue. In addition, BOE alleviated IND-mediated increase in histological score with inhibiting invaded percentage of lesion and restoring mucosa thickness in peri-ulcerative region. BOE increased the gastric tissue bound to Alcian blue and inhibited the decrease in hexose, sialic acid, and collagen levels by IND, suggesting that BOE protects the gastric tissue through preserving mucus and mucosal integrity. Moreover, BOE pre-administration blocked the reduction of prostaglandin E2 and down-regulated histamine and mRNA expression related to secret gastric acid. Furthermore, BOE mitigated inflammatory responses in the gastric tissue by decreasing activity of myeloperoxidase and expression of nuclear factor-κB-dependent inflammatory genes. BOE also suppressed malondialdehyde with preventing the reduction of glutathione, superoxide dismutase, and catalase in the gastric tissue. Therefore, results from present study suggest that BOE will have a potential for preventing gastric injury.

scholarly journals Brassica oleracea Prevents HCl/Ethanol-Induced Gastric Damages in Mice

2020 ◽  
Vol 11 (1) ◽  
pp. 16
Author(s):  
Mi-Ryung Kim ◽  
Tae-Il Kim ◽  
Beom-Rak Choi ◽  
Moon Bong Kim ◽  
Il Je Cho ◽  
...  
Keyword(s):  
Brassica Oleracea ◽  
Gastric Acid ◽  
Nuclear Factor Κb ◽  
Myeloperoxidase Activity ◽  
Mrna Levels ◽  
Gastric Tissue ◽  
Gastric Mucus ◽  
Beneficial Effects ◽  
Wide Range ◽  
Visible Lesion

Brassica oleracea var. capitata L. (cabbage) is a popular vegetable with a wide range of pharmacological activities that help to promote human health. The present study investigated the beneficial effects of B. oleracea var. capitata L. extract (BOE) on HCl/ethanol (H/E)-induced gastric damages in mice. Pre-administration of BOE (25–100 mg/kg) for 7 consecutive days significantly decreased macroscopically visible lesion on the gastric mucosa induced by H/E. In addition, results from hematoxylin and eosin-stained gastric tissue showed that BOE inhibited invaded percentage of lesion and prevented the reduction in mucosal thickness in peri-ulcerative region. BOE significantly alleviated the H/E-mediated decreases in Alcian blue binding, total hexose, sialic acid, and collagen in the gastric tissue, suggesting BOE attenuates the gastric damage via preserving the integrity of gastric mucus. Moreover, BOE significantly decreased histamine level in the plasma and reduced mRNA levels associated with secreting gastric acid. Furthermore, BOE inhibited myeloperoxidase activity and suppressed nuclear factor-κB mRNA and its dependent inflammatory genes expression induced by H/E. BOE also strengthened antioxidant enzyme activity, with a mitigating H/E-mediated increase in malondialdehyde level of the gastric tissue. Thus, these results suggest that BOE has the potential to protect the gastric tissue via inhibiting gastric acid secretion, inflammation, and oxidative stress.

Tanshinone IIA attenuates elastase-induced AAA in rats via inhibition of MyD88-dependent TLR-4 signaling

VASA ◽  
2014 ◽  
Vol 43 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Tao Shang ◽  
Feng Ran ◽  
Qian Qiao ◽  
Zhao Liu ◽  
Chang-Jian Liu
Keyword(s):  
Nuclear Factor Κb ◽  
Tanshinone Iia ◽  
Myeloid Differentiation ◽  
Aortic Tissue ◽  
Toll Like Receptor ◽  
Sprague Dawley ◽  
Toll Like Receptor 4 ◽  
Tissue Samples ◽  
Myeloid Differentiation Factor ◽  
And Control

Background: The purpose of this study was to determine whether myeloid differentiation factor88-dependent Toll-Like Receptor-4 (TLR-4) signaling contributed to the inhibition of abdominal aortic aneurysm (AAA) by Tanshinone IIA (Tan IIA). Materials and methods: Male Sprague-Dawley rats (n = 12 / group) were randomly distributed into three groups: Tan IIA, control, and sham. The rats from Tan IIA and control groups under-went intra-aortic elastase perfusion to induce AAAs, and those in the sham group were perfused with saline. Only the Tan IIA group received Tan IIA (2 mg / rat / d). Aortic tissue samples were harvested at 24 d after perfusion and evaluated using reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry and immunofluorescence. Results: The over-expression of Toll-Like Receptor-4 (TLR-4), Myeloid Differentiation factor 88 (MyD88), Phosphorylated Nuclear Factor κB (pNF-κB) and Phosphorylated IκBα (pIκBα) induced by elastase perfusion were significantly decreased by Tan IIA treatment. Conclusions: Tan IIA attenuates elastase-induced AAA in rats possibly via the inhibition of MyD88-dependent TLR-4 signaling, which may be one potential explanation of why Tan IIA inhibits AAA development through multiple effects.

scholarly journals Preventive Effect of Liupao Tea Polyphenols on HCl/Ethanol-Induced Gastric Injury in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Kai Zhu ◽  
Peng Peng ◽  
Ning Wu ◽  
Xianrong Zhou ◽  
Jianfei Mu ◽  
...  
Keyword(s):  
Gastric Juice ◽  
Tea Polyphenols ◽  
Gastric Injury ◽  
Mouse Serum ◽  
Gastric Tissue ◽  
Preventive Effect ◽  
High Concentration ◽  
Sod Activity ◽  
Bioactive Substances ◽  
Gastric Mucosal Lesions

Liupao tea is a traditional Chinese tea drink. The preventive effect of crude polyphenols in Liupao tea on HCl/ethanol-induced gastric injury was investigated in this study. After a model of gastric injury in mice was established, mouse serum and tissues were analyzed by biochemical and molecular biological methods. The results showed that Liupao tea polyphenols (LTPs) could effectively reduce the area of gastric mucosal lesions, decrease the volume of gastric juice, and increase the pH of gastric juice in mice with gastric injury. Observations of the pathology revealed that LTPs could alleviate cell necrosis and gastric mucosal injury in mice with gastric injury. The SOD activity and GSH level were decreased in mice after gastric injury, while the level of MDA was increased. LTPs could inhibit the changes caused by gastric injury and make the SOD activity, GSH, and MDA levels close to the normal levels. In addition, LTPs could upregulate the mRNA expression of Cu/Zn-SOD, Mn-SOD, CAT, nNOS, and eNOS and downregulate the expression of iNOS in the gastric tissue of mice with gastric injury. Therefore, LTPs can effectively prevent HCl/ethanol-induced gastric injury. HPLC analysis showed that LTP contains six bioactive substances of gallic acid, catechin, caffeine, epicatechin, epigallocatechin gallate, and epicatechin gallate, so the effect of LTP might mainly come from these six components. The effect of a high concentration of LTP is similar to that of ranitidine. LTPs represent a kind of active substance with a protective effect on gastric tissue.

Genotypic differences in nitrogen efficiency of white cabbage (Brassica oleracea L.)

2009 ◽  
Vol 328 (1-2) ◽  
pp. 313-325 ◽  
Author(s):  
Gunda Schulte auf’m Erley ◽  
Elsa Rakhmi Dewi ◽  
Olani Nikus ◽  
Walter J. Horst
Keyword(s):  
Brassica Oleracea ◽  
Nitrogen Efficiency ◽  
Genotypic Differences ◽  
White Cabbage ◽  
Brassica Oleracea L

A Single Intravenous Infusion of Human Choriodecidual Mesenchymal Stem Cell Decreases Early Burn Mortality in a Rodent Model

2021 ◽  
Author(s):  
Eng-Kean Yeong ◽  
Thai-Yen Ling
Keyword(s):  
Intravenous Infusion ◽  
Culture Medium ◽  
Inflammatory Responses ◽  
Total Body Surface Area ◽  
Optimal Dosage ◽  
Sprague Dawley ◽  
Post Injury ◽  
Group B ◽  
Group D ◽  
Single Intravenous Infusion

Abstract Background:Systemic inflammatory responses (SIR) are the main cause of pulmonary dysfunction leading to mortality within hours of extensive burns. Based on previous studies showing that cell entrapment occurs in the lungs following the infusion of human choriodecidual mesenchymal stem cells (hcMSCs), we hypothesize that the intravenous infusion of hcMSCs, with an immunomodulatory potential, will decrease the risk of SIR induced pulmonary failure leading to mortality in burn patients. Methods:Forty adult male Sprague-Dawley rats were randomized into two groups. Group A (sham control, n = 10) received no injury or intervention; the remaining rats (n = 30) were subjected to burns covering 40 % of the total body surface area by immersion of the dorsum in 100 °C water for 15 s under general anesthesia. Injured rats were further randomized into different treatment groups: Group B (saline only control, n = 10), Group C (saline plus culture medium control, n = 10), and Group D (saline plus 2 × 106 hcMSCs, n = 10). Culture medium or hcMSCs were given in a single infusion via the tail vein immediately after burns. Mortality was evaluated on post-burn days 7 and 14. Results:The overall mortality among injured rats was 30 % (9/30). In the first week post-injury, four rats in Group C and three in Group B versus none in Group D died. In the second week, one rat in both Groups C and D died. Altogether, mortality among Group D rats was 10 %, significantly lower than that in groups B and C combined (40 %; p<0.001).Conclusions:We show that a single intravenous infusion of 2 × 106 hcMSCs decreased burn mortality in a severely burned animal model. However, clinical translation requires additional studies to exclude potential adverse effects and to determine the optimal dosage and timing of administration.

CTRP3 protects against uric acid-induced endothelial injury by inhibiting inflammation and oxidase stress in rats

2021 ◽  
pp. 153537022110471
Author(s):  
Junxia Zhang ◽  
Xue Lin ◽  
Jinxiu Xu ◽  
Feng Tang ◽  
Lupin Tan
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Specific Inhibitor ◽  
Endothelial Damage ◽  
Endothelial Injury ◽  
Sprague Dawley ◽  
Protein Levels ◽  
And Oxidative Stress

Hyperuricemia, which contributes to vascular endothelial damage, plays a key role in multiple cardiovascular diseases. This study was designed to investigate whether C1q/tumor necrosis factor (TNF)-related protein 3 (CTRP3) has a protective effect on endothelial damage induced by uric acid and its underlying mechanisms. Animal models of hyperuricemia were established in Sprague-Dawley (SD) rats through the consumption of 10% fructose water for 12 weeks. Then, the rats were given a single injection of Ad-CTRP3 or Ad-GFP. The animal experiments were ended two weeks later. In vitro, human umbilical vein endothelial cells (HUVECs) were first infected with Ad-CTRP3 or Ad-GFP. Then, the cells were stimulated with 10 mg/dL uric acid for 48 h after pretreatment with or without a Toll-like receptor 4 (TLR4)-specific inhibitor. Hyperuricemic rats showed disorganized intimal structures, increased endothelial apoptosis rates, increased inflammatory responses and oxidative stress, which were accompanied by reduced CTRP3 and elevated TLR4 protein levels in the thoracic aorta. In contrast, CTRP3 overexpression decreased TLR4 protein levels and ameliorated inflammatory responses and oxidative stress, thereby improving the morphology and apoptosis of the aortic endothelium in rats with hyperuricemia. Similarly, CTRP3 overexpression decreased TLR4-mediated inflammation, reduced oxidative stress, and rescued endothelial damage induced by uric acid in HUVECs. In conclusion, CTRP3 ameliorates uric acid-induced inflammation and oxidative stress, which in turn protects against endothelial injury, possibly by inhibiting TLR4-mediated inflammation and downregulating oxidative stress.

Effects of matrix metalloproteinase inhibitor on LPS-induced goblet cell metaplasia

2004 ◽  
Vol 287 (1) ◽  
pp. L127-L133 ◽  
Author(s):  
Je Hyeong Kim ◽  
Sung Yong Lee ◽  
Sang Myeon Bak ◽  
In Bum Suh ◽  
Sang Yeub Lee ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Bacterial Infections ◽  
Inflammatory Responses ◽  
Periodic Acid ◽  
Growth Factor Receptor ◽  
Sprague Dawley ◽  
Neutrophilic Infiltration ◽  
Periodic Acid Schiff ◽  
Mucus Hypersecretion ◽  
Egfr Expression

Bacterial infections of the lung are known to induce inflammatory responses, which lead to mucus hypersecretion. Moreover, mucin synthesis in the airways has been reported to be regulated by neutrophilic inflammation-induced epidermal growth factor receptor (EGFR) expression and its activation. Furthermore, matrix metalloproteinases (MMPs), especially MMP-9, have been reported to promote the transmigration of activated neutrophils. In this study, we investigated the associations between lipopolysaccharide (LPS)-induced goblet cell (GC) metaplasia and EGFR expression and the effects of MMP inhibitor (MMPI). Various concentrations of LPS were instilled into the tracheas of pathogen-free Sprague-Dawley rats, and airways were examined at different times after LPS instillation. To examine the role of MMP-9, we treated rats 3 days before LPS instillation and daily thereafter with MMPI. Neutrophilic infiltration, Alcian blue/periodic acid-Schiff (AB/PAS) staining, and immunohistochemical staining for MUC5AC, EGFR, and MMP-9 were performed. The instillation of LPS increased AB/PAS and MUC5AC staining in time- and dose-dependent manners, and treatment with MMPI significantly prevented GC metaplasia. The instillation of LPS into the trachea also induced neutrophilic infiltration and EGFR and MMP-9 expression in the airway epithelium, and MMPI was found to significantly prevent neutrophil recruitment, GC metaplasia, and EGFR and MMP-9 expression. This study demonstrates that the MMP-9 and EGFR cascades are associated with LPS-induced mucus hypersecretion.

scholarly journals Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases

2018 ◽  
Vol 475 (5) ◽  
pp. 839-852 ◽  
Author(s):  
Hiroyuki Nakayama ◽  
Kinya Otsu
Keyword(s):  
Mitochondrial Dna ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Nuclear Factor Κb ◽  
Sterile Inflammation ◽  
Microbial Infection ◽  
Cellular Functions ◽  
Radical Oxygen Species ◽  
Cardiac Inflammation ◽  
Contraction And Relaxation

Mitochondria play a central role in multiple cellular functions, including energy production, calcium homeostasis, and cell death. Currently, growing evidence indicates the vital roles of mitochondria in triggering and maintaining inflammation. Chronic inflammation without microbial infection — termed sterile inflammation — is strongly involved in the development of heart failure. Sterile inflammation is triggered by the activation of pattern recognition receptors (PRRs) that sense endogenous ligands called damage-associated molecular patterns (DAMPs). Mitochondria release multiple DAMPs including mitochondrial DNA, peptides, and lipids, which induce inflammation via the stimulation of multiple PRRs. Among the mitochondrial DAMPs, mitochondrial DNA (mtDNA) is currently highlighted as the DAMP that mediates the activation of multiple PRRs, including Toll-like receptor 9, Nod-like receptors, and cyclic GMP–AMP synthetase/stimulator of interferon gene pathways. These PRR signalling pathways, in turn, lead to the activation of nuclear factor-κB and interferon regulatory factor, which enhances the transcriptional activity of inflammatory cytokines and interferons, and induces the recruitment of inflammatory cells. As the heart is an organ comprising abundant mitochondria for its ATP consumption (needed to maintain constant cyclic contraction and relaxation), the generation of massive amounts of mitochondrial radical oxygen species and mitochondrial DAMPs are predicted to occur and promote cardiac inflammation. Here, we will focus on the role of mtDNA in cardiac inflammation and review the mechanism and pathological significance of mtDNA-induced inflammatory responses in cardiac diseases.

scholarly journals THERAPEUTIC PROFILING OF NANO ENCAPSULATED DIOSGENIN VIA ATTENUATING HORMONAL STATUS, CELL PROLIFERATION, INFLAMMATORY RESPONSES, AND APOPTOSIS IN AN ANIMAL MODEL OF MAMMARY ONCOGENESIS

2021 ◽  
pp. 126-132
Author(s):  
MANOBHARATHI VENGAIMARAN ◽  
KALAIYARASI DHAMODHARAN ◽  
MIRUNALINI SANKARAN
Keyword(s):  
Cell Proliferation ◽  
Molecular Docking ◽  
Cyclin D1 ◽  
Inflammatory Responses ◽  
Chitosan Nanoparticles ◽  
Hormonal Status ◽  
Sprague Dawley ◽  
Therapeutic Impact ◽  
Sprague Dawley Rats ◽  
Tnf Α

Objective: The central motive of this study is to explore the therapeutic impact of Diosgenin encapsulated Chitosan nanoparticles (DG@CS-NP) on mammary carcinogenesis in female Sprague Dawley rats via modulating hormonal status, cell proliferation, inflammatory responses, and Apoptosis. Methods: 7,12-dimethylbenz(a)anthracene (DMBA) was administered subcutaneously near the mammary gland (25 mg/kg b. wt) to provoke mammary tumor in female Sprague Dawley rats. Following the progress of a tumor, DMBA-induced tumor-bearing rats were medicated orally with 5 mg/kg b. wt of DG@CS-NP. Consequently, the expression of ER, PR, PCNA, Cyclin D1, NF-κB, TNF-α, Bcl-2, Caspases-3, and p53 in experimental rats were revealed via architectural immunohistochemistry. Further, Diosgenin interactions with these proteins were evidently confirmed by molecular docking analysis. Results: As a result, we noticed diminished levels of ER, PR, PCNA, Cyclin D1, NF-κB, TNF-α, and Bcl-2 expressions in DG@CS-NP medicated rats as well as with elevated levels of Caspases-3 and p53 expressions. In DMBA rats, the expressions were vice versa. Additionally, molecular docking analyses support these outcomes by highlighting the strong interaction between Diosgenin and breast cancer targets. Conclusion: These reports prove that DG@CS-NP imposes its therapeutic impact by hormonal adjustments, downregulating proteins involved in inflammation and cellular proliferation, and thereby promotes apoptosis by impeding apoptotic inhibitors.

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