scholarly journals Protective effect of snail secretion filtrate against ethanol-induced gastric ulcer in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Enrico Gugliandolo ◽  
Marika Cordaro ◽  
Roberta Fusco ◽  
Alessio Filippo Peritore ◽  
Rosalba Siracusa ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Inflammatory Response ◽  
Protective Effect ◽  
Underlying Mechanism ◽  
New Drugs ◽  
Ethanol Administration ◽  
Common Disease ◽  
Intragastric Administration ◽  
Human Disorders ◽  
Interest In Research

AbstractGastric ulcer or peptic ulcer is a common disease worldwide. Basically, it develops when there is an imbalance between the protective and aggressive factors, especially at the luminal surface of epithelial cells. Thus, there is a constant interest in research new drugs for treatment of gastric ulcer. The snail secretion is a dense mucous, that covers the external surface of the snails, with important functions for the survival of snails. The biological proprieties of snail Helix Aspersa Muller mucus it has been known for centuries to treat human disorders in particular for skin disease. Recently the use of snail mucus has seen a worldwide increase, as a component in cosmetic product and it has been used in particular for the management of wound and skin disorders. In this study we use a murine model of ethanol intragastric administration which has been widely used to test the drugs efficacies and to explore the underlying mechanism for gastric ulcer development. The intragastric ethanol administration causes several mucosal damages and an induction of a severe inflammatory response. Our results show a significant protective effect of snail secretion filtrate in reducing macroscopic and histological lesions, as well the protective effect on mucus content, oxidative stress and inflammatory response. In conclusion this study demonstrate the protective effect of intragastrical snail secretion filtrate, in a model of ethanol-induced gastric ulcer in mice, suggesting its possible useful use in the treatment or prevention of gastric ulcer.

Protective effect of the new compound — salicyl-carnosine — on the formation of chronic acetate gastric ulcer in rats*

2019 ◽  
Vol 163 (3) ◽  
pp. 58-64
Author(s):  
I.E. Trubitsyna ◽  
◽  
S.L. Stvolinsky ◽  
O.I. Kulikova ◽  
T.N. Fedorova ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Protective Effect

scholarly journals SIRT1 attenuates sepsis-induced acute kidney injury via Beclin1 deacetylation-mediated autophagy activation

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhiya Deng ◽  
Maomao Sun ◽  
Jie Wu ◽  
Haihong Fang ◽  
Shumin Cai ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Cell Model ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Autophagy Induction ◽  
Promising Therapeutic Approach ◽  
Related Proteins ◽  
Caecal Ligation And Puncture

AbstractOur previous studies showed that silent mating-type information regulation 2 homologue-1 (SIRT1, a deacetylase) upregulation could attenuate sepsis-induced acute kidney injury (SAKI). Upregulated SIRT1 can deacetylate certain autophagy-related proteins (Beclin1, Atg5, Atg7 and LC3) in vitro. However, it remains unclear whether the beneficial effect of SIRT1 is related to autophagy induction and the underlying mechanism of this effect is also unknown. In the present study, caecal ligation and puncture (CLP)-induced mice, and an LPS-challenged HK-2 cell line were established to mimic a SAKI animal model and a SAKI cell model, respectively. Our results demonstrated that SIRT1 activation promoted autophagy and attenuated SAKI. SIRT1 deacetylated only Beclin1 but not the other autophagy-related proteins in SAKI. SIRT1-induced autophagy and its protective effect against SAKI were mediated by the deacetylation of Beclin1 at K430 and K437. Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. Our study was the first to demonstrate the important role of SIRT1-induced Beclin1 deacetylation in autophagy and its protective effect against SAKI. These findings suggest that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.

scholarly journals Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1

2020 ◽  
Vol 15 (1) ◽  
pp. 544-552
Author(s):  
Xiaoyan Deng ◽  
Zhixing Lin ◽  
Chao Zuo ◽  
Yanjie Fu
Keyword(s):  
Inflammatory Response ◽  
Underlying Mechanism ◽  
Notch Receptor ◽  
Raw264.7 Cells ◽  
Luciferase Reporter ◽  
Raw264.7 Macrophages ◽  
Factor Α ◽  
Anti Inflammation ◽  
Necrosis Factor ◽  
Dual Luciferase Reporter Assay

AbstractCirculating miR-150-5p has been identified as a prognostic marker in patients with critical illness and sepsis. Herein, we aimed to further explore the role and underlying mechanism of miR-150-5p in sepsis. Quantitative real-time-PCR assay was performed to detect the expression of miR-150-5p upon stimulation with lipopolysaccharide (LPS) in RAW264.7 cells. The levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β were measured by ELISA assay. Cell apoptosis was determined using flow cytometry. Western blot was used to assess notch receptor 1 (Notch1) expression in LPS-induced RAW264.7 cells. Dual-luciferase reporter assay was employed to validate the target of miR-150-5p. Our data showed that miR-150-5p was downregulated and Notch1 was upregulated in LPS-stimulated RAW264.7 cells. miR-150-5p overexpression or Notch1 silencing alleviated LPS-induced inflammatory response and apoptosis in RAW264.7 cells. Moreover, Notch1 was a direct target of miR-150-5p. Notch1 abated miR-150-5p-mediated anti-inflammation and anti-apoptosis in LPS-induced RAW264.7 cells. miR-150-5p alleviated LPS-induced inflammatory response and apoptosis at least partly by targeting Notch1 in RAW264.7 cells, highlighting miR-150-5p as a target in the development of anti-inflammation and anti-apoptosis drugs for sepsis treatment.

scholarly journals Flaxseed orbitides, linusorbs, inhibit LPS-induced THP-1 macrophage inflammation

RSC Advances ◽  
2020 ◽  
Vol 10 (38) ◽  
pp. 22622-22630
Author(s):  
Xian-Guo Zou ◽  
Youn Young Shim ◽  
Jae Youl Cho ◽  
Deok Jeong ◽  
Jian Yang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cyclic Peptides ◽  
Underlying Mechanism ◽  
Anti Inflammatory

Linusorbs (flax orbitides) are a family of plant cyclic peptides. We investigate the anti-inflammatory activities of two different linusorbs ([1–9-NaC]-linusorb B2 and [1–9-NaC]-linusorb B3) and the underlying mechanism of this inflammatory response.

Conflict of Interest in Research and Publication: Has the Pendulum Swung Too Far?

2021 ◽  
Author(s):  
Caroline Glicksman
Keyword(s):  
Conflict Of Interest ◽  
International Association ◽  
New Drugs ◽  
Work Effort ◽  
Disclosure Requirements ◽  
Academic Researchers ◽  
Potential Benefits ◽  
Interest In Research ◽  
Medical Articles

Abstract Traditionally there has been a collaboration between scientists and industry contributing to the development of new drugs, biologics, and medical devices. Conflict-of-interest (COI) may develop amongst surgeons and academic researchers especially during the process of refinement of techniques and the marketing and sale of devices. Dramatic examples of COI occurred over the last fifty years leading to strict regulations designed to reduce COI at research institutions. Action taken by the International Association of Medical Journal Editors (ICMJE) created COI guidelines to help authors and editors to ensure clear, reproducible, and unbiased medical articles. The Physicians Payments Sunshine Act was designed to increase transparency of financial relationships between physicians and industry. However, there are instances where authors and scientists are not obligated to fully disclose their COI. Only direct payments are required to be reported, not indirect payments to faculty at large academic institutions, allowing some to take advantage of the exceptions to the disclosure requirements while others must disclose payment for their work effort. Based on prominent scandals, regulations aimed at reducing industry influence in research and publication may fail to recognize the potential benefits of collaboration and produce a narrow-minded view of trust. Where should an editorial board or an academic institution draw the line?

scholarly journals The Protective Effect of Total Flavones from Rhododendron simsii Planch. on Myocardial Ischemia/Reperfusion Injury and Its Underlying Mechanism

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Sheng-Yong Luo ◽  
Qing-Hua Xu ◽  
Gong Peng ◽  
Zhi-Wu Chen
Keyword(s):  
Myocardial Infarction ◽  
Protective Effect ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Assay Method ◽  
Protective Effects ◽  
Rhododendron Simsii ◽  
Rhoa Activity ◽  
Protein Expressions

Objectives. Total flavones from Rhododendron simsii Planch. (TFR) are the effective part extracted from the flowers of Rhododendron simsii Planch. and have obvious protective effects against cerebral ischemic or myocardial injuries in rabbits and rats. However, their mechanism of cardioprotection is still unrevealed. Therefore, the present study was designed to investigate the effect of TFR on myocardial I/R injury and the underlying mechanism. Methods. TFR groups were treated by gavage once a day for 3 days at a dose of 20, 40, and 80 mg/kg, respectively, and then the model of myocardial I/R injury was established. Myocardial infarction, ST-segment elevation, and the expression of UTR, ROCK1, ROCK2, and p-MLC protein in rat myocardium were determined at 90 min after reperfusion. UTR siRNA in vivo transfection and competition binding assay method were used to study the relationship between the protective effect of TFR and UTR. Results. The expression of UTR protein markedly decreased in myocardium of UTR siRNA transfection group rats. TFR could significantly reduce the infarct size and inhibit the increase of RhoA activity and ROCK1, ROCK2, and p-MLC protein expressions both in WT and UTR knockdown rats. The reducing rate of TFR in myocardial infarction area, RhoA activity, and ROCK1, ROCK2, and p-MLC protein expressions in UTR knockdown rats decreased markedly compared with that in WT rats. In addition, TFR had no obvious effect on the increase of ΣST in UTR knockdown rats in comparison with that in model group. In particular, TFR could significantly inhibit the combination of [I125]-hu-II and UTR, and IC50 was 0.854 mg/l. Conclusions. The results indicate that the protective effect of TFR on I/R injury may be correlated with its blocking UTR and the subsequent inhibition of RhoA/ROCK signaling pathway.

A comparative study on the possible protective effect of esomeprazole, spirulina, wheatgrass on indomethacin-induced gastric ulcer in male albino rats

2019 ◽  
Vol 46 (5) ◽  
pp. 4843-4860 ◽  
Author(s):  
Amy Fakhry Boushra ◽  
Asmaa Mohammed Elsayed ◽  
Noha Abdellatif Ibrahim ◽  
Maha Khaled Abdelwahed ◽  
Eman Ibrahim Ahmed
Keyword(s):  
Gastric Ulcer ◽  
Comparative Study ◽  
Protective Effect ◽  
Albino Rats

scholarly journals Effects of Xiang Sha Yang Wei Wan on Ethanol-Induced Gastric Ulcer in Sprague Dawley Rats: a Histological Study

2020 ◽  
Vol 12 (2) ◽  
Author(s):  
Al-Qaraghuli AMS ◽  
Abdel Wahab EMN ◽  
Al-Ani IM ◽  
Faisal GG
Keyword(s):  
Gastric Ulcer ◽  
Oral Dose ◽  
Histological Study ◽  
Treated Group ◽  
Ethanol Administration ◽  
Gastric Mucosal Lesion ◽  
Sprague Dawley ◽  
Group I ◽  
Sprague Dawley Rats ◽  
Group Ii

Introduction: Xiang Sha Yang Wei Wan (XSYWW) is a Chinese traditional medicine that is used for gastrointestinal disorders, specifically gastric ulcer in many countries of South-East Asia. The aim of the study was to evaluate the potential effects of XSYWW on ethanol-induced gastric ulcer in rats by means of histological Study. On a similar basis of treatment, ranitidine, a conventional medication was used as gold standard. Methods: Fifty five male Sprague-Dawley rats (250-300 gm) were divided into four groups. Group I (ethanol treated group) was the control group and gastric ulcers were induced by administering 100% ethanol (1 ml/200 g). Group II (Pre-treatment group) was divided into two subgroups; they were orally fed with 1.0 gm/kg and 2.0 gm/kg respectively of XSYWW solution. Thirty minutes later they were administered with absolute ethanol as in group I. Group III, was given an oral dose of 2gm/kg of XSYWW solution after one hour of ethanol administration. Group IV was given an oral dose of 200mg/kg ranitidine solution after one hour of ethanol administration. Five rats from groups I, III and IV were sacrificed on day 1, 2 and 3 while the animals of group II were sacrificed one hour after ethanol administration. Results: Histological study of the stomachs from ethanol treated rats showed multiple ulcers of various depths that reached the muscularis and the serosa. Conclusion: Pre or post-treated rats with XSYWW showed that XSYWW has protective effect against ethanol-induced gastric mucosal lesion. However, there was a faster and more complete healing process in the ranitidine treated group when compared to the XSYWW treated subjects.

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