scholarly journals Protective Effects of Curcumin and its Nano-Phytosome on Carrageenan-Induced Inflammation in Mice Model: Behavioral and Biochemical Responses

2020 ◽  
Vol Volume 13 ◽  
pp. 45-51 ◽  
Author(s):  
Saeideh Baradaran ◽  
Akbar Hajizadeh Moghaddam ◽  
Sedigheh Khanjani Jelodar ◽  
Nasroallah Moradi-kor
Keyword(s):  
Protective Effects ◽  
Mice Model ◽  
Biochemical Responses

scholarly journals Probiotic and Functional Properties of Limosilactobacillus reuteri INIA P572

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1860
Author(s):  
Patricia Diez-Echave ◽  
Izaskun Martín-Cabrejas ◽  
José Garrido-Mesa ◽  
Susana Langa ◽  
Teresa Vezza ◽  
...  
Keyword(s):  
In Vitro Assays ◽  
Immunomodulatory Activity ◽  
Probiotic Properties ◽  
Protective Effects ◽  
Mice Model ◽  
In Vivo Models ◽  
Food Borne ◽  
Gastrointestinal Conditions

Limosilactobacillus reuteri INIA P572 is a strain able to produce the antimicrobial compound reuterin in dairy products, exhibiting a protective effect against some food-borne pathogens. In this study, we investigated some probiotic properties of this strain such as resistance to gastrointestinal passage or to colonic conditions, reuterin production in a colonic environment, and immunomodulatory activity, using different in vitro and in vivo models. The results showed a high resistance of this strain to gastrointestinal conditions, as well as capacity to grow and produce reuterin in a human colonic model. Although the in vitro assays using the RAW 264.7 macrophage cell line did not demonstrate direct immunomodulatory properties, the in vivo assays using a Dextran Sulphate Sodium (DSS)-induced colitic mice model showed clear immunomodulatory and protective effects of this strain.

Protective effects of recombinant glycoprotein D based prime boost approach against duck enteritis virus in mice model

2015 ◽  
Vol 88 ◽  
pp. 78-86 ◽  
Author(s):  
S. Aravind ◽  
Nitin Machindra Kamble ◽  
Satish S. Gaikwad ◽  
Sanjeev Kumar Shukla ◽  
R. Saravanan ◽  
...  
Keyword(s):  
Duck Enteritis Virus ◽  
Protective Effects ◽  
Glycoprotein D ◽  
Mice Model ◽  
Recombinant Glycoprotein ◽  
Enteritis Virus

scholarly journals Tropisetron Protects Against Acetaminophen-Induced Liver Injury via Suppressing Hepatic Oxidative Stress and Modulating the Activation of JNK/ERK MAPK Pathways

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Fu-Chao Liu ◽  
Hung-Chen Lee ◽  
Chia-Chih Liao ◽  
Allen H. Li ◽  
Huang-Ping Yu
Keyword(s):  
Liver Injury ◽  
Map Kinases ◽  
Dependent Manner ◽  
Protective Effects ◽  
Mice Model ◽  
Terminal Protein ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Hepatic Lipid Peroxidation ◽  
Dose Dependent

Objectives. To investigate the protective effects of tropisetron on acetaminophen- (APAP-) induced liver injury in a mice model.Methods. C57BL/6 male mice were given tropisetron (0.3 to 10 mg/kg) 30 minutes before a hepatotoxic dose of acetaminophen (300 mg/kg) intraperitoneally. Twenty hours after APAP intoxication, sera alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, hepatic myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) activities, and liver histopathological changes were examined. The MAP kinases were also detected by western blotting.Results. Our results showed that tropisetron pretreatment significantly attenuated the acute elevations of the liver enzyme ALT level, hepatic MPO activity, and hepatocytes necrosis in a dose-dependent manner (0.3–10 mg/kg) in APAP-induced hepatotoxicity mice. Tropisetron (1 and 3 mg/kg) suppressed APAP-induced hepatic lipid peroxidation expression and alleviated GSH and SOD depletion. Administration of tropisetron also attenuated the phosphorylation of c-Jun-NH2-terminal protein kinase (JNK) and extracellular signal-regulated kinase (ERK) caused by APAP.Conclusion. Our data demonstrated that tropisetron’s hepatoprotective effect was in part correlated with the antioxidant, which were mediated via JNK and ERK pathways on acetaminophen-induced liver injury in mice.

scholarly journals Dietary Purple Potato Supplementation Ameliorates Gut Inflammation and Associated Colitis

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 535-535
Author(s):  
Shima Bibi ◽  
Yansong Xue ◽  
Yang He ◽  
Min Du ◽  
Boon Chew ◽  
...  
Keyword(s):  
Control Diet ◽  
Goblet Cells ◽  
Protective Effects ◽  
Mice Model ◽  
Differentiation Markers ◽  
Beneficial Effects ◽  
Funding Sources ◽  
Epithelial Structure ◽  
Biochemical Analyses ◽  
Deficient Mice

Abstract Objectives The incidence of inflammatory bowel disease (IBD) is rapidly increasing worldwide. Patients with IBD experience increased susceptibility to colorectal cancer and are associated with morbidity and mortality. Diets are known factors associated with IBD. This study examined the beneficial effects of dietary purple potato against spontaneous colitis and improving gut microbiota in interleukin (IL)-10-deficient mice, a commonly used IBD mice model. Methods IL-10-deficient mice at 7-week-old were assigned to a standard rodent diet (CON) or a control diet supplemented with 10% purple potato (dry feed weight) for 11 weeks, when colonic tissues were collected for histological and biochemical analyses. Results Purple potato supplementation had no effect on feed intake and body weight in IL-10-deficient mice during the 11-week feeding trial. Purple potato supplementation improved the colitis symptom and the integrity of the colonic epithelial structure with reduced inflammation and pathological scores. Furthermore, the density of goblet cells and differentiation markers for goblet cells was enhanced due to PP supplementation. Conclusions Data collectively showed that dietary purple potato supplementation had protective effects against colitis onset in IL-10-deficient mice and improved gut epithelial structure, providing a promising dietary approach for the management and prevention of colitis. Funding Sources USDA-NIFA and Northwest Potato Research Consortium.

scholarly journals Qing-Re-Xiao-Zheng Formula Modulates Gut Microbiota and Inhibits Inflammation in Mice With Diabetic Kidney Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Yabin Gao ◽  
Ruibing Yang ◽  
Lan Guo ◽  
Yaoxian Wang ◽  
Wei Jing Liu ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Gut Microbiota ◽  
Diabetic Kidney Disease ◽  
Inflammatory Responses ◽  
Protective Effects ◽  
Mice Model ◽  
Diabetic Kidney ◽  
Metabolic Inflammation ◽  
Gut Microbiota Dysbiosis

Evidence indicates that the metabolic inflammation induced by gut microbiota dysbiosis contributes to diabetic kidney disease. Prebiotic supplementations to prevent gut microbiota dysbiosis, inhibit inflammatory responses, and protect the renal function in DKD. Qing-Re-Xiao-Zheng formula (QRXZF) is a Traditional Chinese Medicine (TCM) formula that has been used for DKD treatment in China. Recently, there are growing studies show that regulation of gut microbiota is a potential therapeutic strategy for DKD as it is able to reduce metabolic inflammation associated with DKD. However, it is unknown whether QRXZF is effective for DKD by regulating of gut microbiota. In this study, we investigated the reno-protective effect of QRXZF by exploring its potential mechanism between gut microbiota and downstream inflammatory pathways mediated by gut-derived lipopolysaccharide (LPS) in the kidney. High-fat diet (HFD) and streptozotocin injection-induced DKD mice model was established to assess the QRXZF effect in vivo. Mice treated with QRXZF for 8 weeks had significantly lower levels of urinary albumin, serum cholesterol and triglycerides. The renal injuries observed through histological analysis were attenuated as well. Also, mice in the QRXZF group had higher levels of Zonula occludens protein-1 (ZO-1) expression, lower levels of serum fluorescein-isothiocyanate (FITC)-dextran and less-damaged colonic mucosa as compared to the DKD group, implying the benefit role for the gut barrier integrity. QRXZF treatment also reversed gut dysbiosis and reduced levels of gut-derived LPS. Notably, the expression of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB), which are important inflammation pathways in DKD, were suppressed in the QRXZF groups. In conclusion, our results indicated that the reno-protective effects of QRXZF was probably associated with modulating gut microbiota and inhibiting inflammatory responses in the kidney.

scholarly journals DKK3 attenuates JNK and AP-1 induced inflammation via Kremen-1 and DVL-1 in mice following intracerebral hemorrhage

2019 ◽  
Author(s):  
Yang Xu ◽  
Derek Nowrangi ◽  
Hui Liang ◽  
Tian Wang ◽  
Lingyan Yu ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Activator Protein 1 ◽  
Protective Effects ◽  
Mice Model ◽  
Stroke Subtype ◽  
Male Adult ◽  
Neurological Outcomes ◽  
Collagenase Injection ◽  
Neurobehavioral Deficits

Abstract Background Intracerebral hemorrhage (ICH) is the most devastating stroke subtype, with a poor prognosis and few proven treatments. Neuroinflammation is associated with ICH-induced brain injury and unfavorable outcomes. There is growing evidence that dinkkopf (DKK) 3 plays a key role in the adaptive anti-inflammatory and neuroprotective responses following intracerebral hemorrhage. This study aimed to evaluate the protective effects of DKK3 against brain edema and neuroinflammation in a mice model of ICH.Methods Male, adult CD1 mice were subjected to sham or ICH surgery using a collagenase injection model. ICH animals received either recombinant DKK3, Kremen-1 siRNA, or DVL-1 siRNA. The neurobehavioral deficits were evaluated at 24 h, 72 h, and 28 days after ICH induction. Western blot and immunofluorescence were employed to examine the expression and localization of DKK3, Kremen-1, Dishevelled-1 (DVL-1), c-JUN N-terminal kinase (JNK), Activator protein-1 (AP-1), cleaved caspase-1, NF-κB, and IL-1β in the brain.Results The expression of endogenous DKK3 and DVL-1 was transiently decreased after ICH compared to that in the sham group. Compared to the mice of ICH, exogenous rDKK3 administration reduced the brain water content and affected the neurological functions in ICH mice. Moreover, DKK3 was colocalized with Kremen-1 in microglia. Using a Kremen-1 or DVL-1 siRNA-induced in vivo knockdown approach, we demonstrated that the effects of DKK3 against ICH were mediated, at least partly, by the Kremen-1 and DVL-1 pathways.Conclusions DKK3 improves the neurological outcomes, potentially by decreasing JNK/AP-1 mediated inflammation, thereby ameliorating the short- and long-term sequelae after ICH.

scholarly journals The Protective Effects of Astaxanthin on the OVA-Induced Asthma Mice Model

Molecules ◽  
2017 ◽  
Vol 22 (11) ◽  
pp. 2019 ◽  
Author(s):  
Yun-Ho Hwang ◽  
Seong-Gyeol Hong ◽  
Seul-Ki Mun ◽  
Su-Jin Kim ◽  
Sung-Ju Lee ◽  
...  
Keyword(s):  
Protective Effects ◽  
Mice Model

Glatiramer acetate treatment inhibits inflammatory responses and improves survival in a mice model of cecal ligation and puncture-induced sepsis

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Elahe Maleki ◽  
Mohammad Sheibani ◽  
Sadaf Nezamoleslami ◽  
Ahmad Reza Dehpour ◽  
Nasrin Takzaree ◽  
...  
Keyword(s):  
Survival Rate ◽  
Glatiramer Acetate ◽  
Inflammatory Cytokines ◽  
Cecal Ligation ◽  
Protective Effects ◽  
Cecal Ligation And Puncture ◽  
Mice Model ◽  
Term Survival ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Abstract Objectives Sepsis is a clinical crisis which has been considered as one of the important causes of mortality across the world. We hypothesized that modulation of hyper-inflammatory phase of sepsis pathophysiology can lead to protective effects on survival outcome. Glatiramer acetate (GA) is a neuroprotective drug commonly used in multiple sclerosis (MS). GA is characterized by immunom activity via regulation of innate and adaptive immunity. This study was designed to evaluate the acute treatment with GA on initial inflammatory response-induced mortality in septic mice. Methods Cecal ligation and puncture (CLP) model was operated on male mice as a model of Polymicrobial sepsis. GA was administrated intraperitoneally after the sepsis induction at doses of 0.5, 1, and 2 mg/kg in three treatment groups. To investigate the effect of GA on short-term survival, septic mice were observed during 72 h after CLP. Serum levels of TNF-α, IL-1β, and IL-6 as pro-inflammatory cytokines and also IL-10 as a critical anti-inflammatory cytokine were analysed. To consider sepsis-induced acute kidney injury, renal functional biomarkers and histopathological changes was assessed. Results GA treatment significantly improved survival rate at doses of 1, and 2 mg/kg. Survival improvement was accompanied by remarkable reduction in the pro-inflammatory cytokines and enhanced production of IL-10. GA showed to have protective effects on renal function as well. Conclusions Immunomodulatory and anti-inflammatory properties of GA resulted in increase in survival rate and decrease in inflammatory markers in mice model of cecal ligation and puncture–induced sepsis.

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