The protective effect of vitexinin septic encephalopathy by reducing leukocyte-endothelial adhesion and inflammatory response

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.

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Protective effect of a novel Rho kinase inhibitor WAR–5 in experimental autoimmune encephalomyelitis by modulating inflammatory response and neurotrophic factors

Experimental and Molecular Pathology ◽

10.1016/j.yexmp.2015.06.016 ◽

2015 ◽

Vol 99 (2) ◽

pp. 220-228 ◽

Cited By ~ 11

Author(s):

Yan-hua Li ◽

Jie-zhong Yu ◽

Yan-le Xin ◽

Ling Feng ◽

Zhi Chai ◽

...

Keyword(s):

Inflammatory Response ◽

Experimental Autoimmune Encephalomyelitis ◽

Protective Effect ◽

Neurotrophic Factors ◽

Kinase Inhibitor ◽

Rho Kinase ◽

Autoimmune Encephalomyelitis ◽

Rho Kinase Inhibitor ◽

Experimental Autoimmune

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Umbelliferone alleviates hepatic injury in diabetic db/db mice via inhibiting inflammatory response and activating Nrf2-mediated antioxidant

Bioscience Reports ◽

10.1042/bsr20180444 ◽

2018 ◽

Vol 38 (4) ◽

Cited By ~ 9

Author(s):

Jiangning Yin ◽

Hanqing Wang ◽

Guoyuan Lu

Keyword(s):

Blood Glucose ◽

Inflammatory Response ◽

Protective Effect ◽

High Mobility ◽

Hepatic Function ◽

Tolerance Test ◽

Oral Glucose ◽

Stress Indicators ◽

Tnf Α ◽

Oxidative Stress Indicators

The current study was designed to investigate the protective effect and possible mechanisms of umbelliferone (Umb) on liver injury in diabetic C57BL/KsJ-db/db (dbdb) mice. Mice were divided into five groups: wild-type mice group (WY), dbdb mice group, dbdb mice + Metformin (100 mg/kg) group, dbdb mice + Umb (20, 40 mg/kg) group. Blood glucose regulation was assessed by an oral glucose tolerance test (OGTT). At 28 days after drug administration, blood samples were obtained for the analysis of lipids and enzymes related to hepatic function, including alanine aminotransferase (ALT), aspartate aminotransaminase (AST) and total cholesterol (TC) and triglyceride (TG). Expression levels of inflammatory cytokines (TNF-α, IL-1β, and IL-6) and oxidative stress indicators (SOD and MDA) were measured with ELISA kit. The expressions of high-mobility group box 1 (HMGB1), Toll-like receptor (TLR) 4 (TLR4), Myd88, NF-κB, IκB, Nrf2, and HO-1 proteins were also evaluated by Western blotting analysis. The results showed that Umb significantly restored the blood glucose in OGTT, and inhibited the levels of insulin, TG, TC, as well as activities of ALT and AST. Moreover, Umb inhibited diabetic inflammation through down-regulating the expression of HMGB1, TLR4, NF-κB, and IκB. In addition, Umb alleviated oxidative damage in the liver by activating Nrf2-mediated signal pathway. These findings demonstrated that Umb exhibited protective effect against diabetic live injury, which may be through inhibiting HMGB1-induced inflammatory response and activating Nrf2-mediated antioxidant.

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The Protective Effect of Picroside II on Isoflurane-Induced Neuronal Injury in Rats via Downregulating miR-195

NeuroImmunoModulation ◽

10.1159/000519779 ◽

2021 ◽

pp. 1-9

Author(s):

Hui Li ◽

Weijia Du ◽

Yawei Yuan ◽

Jingjing Xue ◽

Qiang Li ◽

...

Keyword(s):

Inflammatory Response ◽

Protective Effect ◽

Inflammatory Cytokines ◽

Escape Latency ◽

Neuronal Cells ◽

Neuronal Injury ◽

Morris Water Maze Test ◽

Picroside Ii ◽

Tnf Α ◽

Pro Inflammatory Cytokines

Introduction: Numerous pieces of evidence demonstrated that isoflurane induces hippocampal cell injury and cognitive impairments. Picroside II has been investigated for its anti-apoptosis and antioxidant neuroprotective effects. We aimed to explore the protective effects of picroside II and the role of microRNA-195 (miR-195) on isoflurane-induced neuronal injury in rats. Methods: The Morris water maze test was used to evaluate the effects of isoflurane on rats regarding escape latency and time in quadrant parameters. Real-time quantitative PCR was used to detect the expression levels of miR-195 and pro-inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) mRNA, in the hippocampal tissues and neuronal cells. Results: The picroside II significantly improves isoflurane-induced higher escape latency and lower time spent in the quadrant compared with the control rats. Picroside II also promotes cell viability and suppresses cell apoptosis of isoflurane-induced neuronal cells. Besides, picroside II suppresses the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) and miR-195 in vivo and in vitro. Furthermore, overexpression of miR-195 abrogates the effects of picroside II on the expression of pro-inflammatory cytokines. The appropriate dose of picroside II is 20 mg/kg. Conclusion: Picroside II could protect the nervous system possibly through inhibiting the inflammatory response in the isoflurane-induced neuronal injury of rats. The protective effect of picroside II may be achieved by downregulating the expression of miR-195 and then inhibiting the inflammatory response.

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Protective Effect of Tetrandrine on Sodium Taurocholate-Induced Severe Acute Pancreatitis

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2015/129103 ◽

2015 ◽

Vol 2015 ◽

pp. 1-8 ◽

Cited By ~ 3

Author(s):

Xian-lin Wu ◽

Jie-xing Li ◽

Zhen-dong Li ◽

Da-sheng Liu ◽

Su-hong Lu ◽

...

Keyword(s):

Acute Pancreatitis ◽

Free Radical ◽

Bile Duct ◽

Systemic Inflammatory Response Syndrome ◽

Inflammatory Response ◽

Protective Effect ◽

Severe Acute Pancreatitis ◽

Sodium Taurocholate ◽

Multiple Organ ◽

Multiple Organ Dysfunction

Tet is a type of alkaloid extracted fromStephania tetrandra, and it has recently been demonstrated that Tet can protect against inflammation and free radical injury and inhibit the release of inflammatory mediators. The present study was designed to observe the protective effect of Tet on sodium taurocholate-induced severe acute pancreatitis (SAP). The rat model of SAP was induced by retrograde bile duct injection of sodium taurocholate and then treated with Verapamil and Tet. The results showed that Tet can reduce NF-κB activation in pancreas issue, inhibit the SAP cascade, and improve SAP through inducing pancreas acinar cell apoptosis and stabilizing intracellular calcium in the pancreas, thus mitigating the damage to the pancreas. Our study revealed that Tet may reduce systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndromes (MODS) to protect against damage, and these roles may be mediated through the NF-κB pathway to improve the proinflammatory/anti-inflammatory imbalance.

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