scholarly journals Effect ofAngelica sinensisPolysaccharides on OsteoarthritisIn VivoandIn Vitro: A Possible Mechanism to Promote Proteoglycans Synthesis

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Jun Qin ◽  
Yan-song Liu ◽  
Jun Liu ◽  
Jing Li ◽  
Yang Tan ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Articular Chondrocytes ◽  
Interleukin 1 ◽  
Knee Joints ◽  
Protective Effects ◽  
Interleukin 1 Beta ◽  
Degrading Enzymes ◽  
Matrix Degrading Enzymes

This study investigated the effect ofAngelica sinensispolysaccharides (APS-3c) on rat osteoarthritis (OA) modelin vivoand rat interleukin-1-beta- (IL-1β-) stimulated chondrocytesin vitro. APS-3c was administrated into rat OA knee joints and had protective effects on rat OA cartilagein vivo. Primary rat articular chondrocytes were cotreated with APS-3c and IL-1β  in vitro. 2~50 μg/mL APS-3c had no effect on chondrocytes viability, whereas it increased the proteoglycans (PGs) synthesis inhibited by IL-1β. Microarray analysis showed that the significant changes were concentrated in the genes which were involved in PGs synthesis. RT-PCR confirmed that treatment with APS-3c increased the mRNA expression of aggrecan and glycosyltransferases (GTs) inhibited by IL-1βbut did not affect the mRNA expression of matrix-degrading enzymes. These results indicate that APS-3c can improve PGs synthesis of chondrocytes on rat OA modelin vivoand IL-1β-stimulated chondrocytesin vitro, which is due to the promotion of the expression of aggrecan and GTs involved in PGs synthesis but not the inhibition of the expression of matrix-degrading enzymes. Our findings suggest the clinical relevance of APS-3c in the prospective of future alternative medical treatment for OA.

Healing effects of curcumin nanoparticles in deep tissue injury mouse model.

2020 ◽  
Vol 18 ◽  
Author(s):  
Zirui Zhang ◽  
Shangcong Han ◽  
Panpan Liu ◽  
Xu Yang ◽  
Jing Han ◽  
...  
Keyword(s):  
Wound Healing ◽  
Mrna Expression ◽  
Tissue Injury ◽  
Inflammatory Cells ◽  
Pcr Analysis ◽  
Protective Effects ◽  
Deep Tissue ◽  
Deep Tissue Injury

Background: Chronic inflammation and lack of angiogenesis are the important pathological mechanisms in deep tissue injury (DTI). Curcumin is a well-known anti-inflammatory and antioxidant agent. However, curcumin is unstable under acidic and alkaline conditions, and can be rapidly metabolized and excreted in the bile, which shortens its bioactivity and efficacy. Objective: This study aimed to prepare curcumin-loaded poly (lactic-co-glycolic acid) nanoparticles (CPNPs) and to elucidate the protective effects and underlying mechanisms of wound healing in DTI models. Methods: CPNPs were evaluated for particle size, biocompatibility, in vitro drug release and their effect on in vivo wound healing. Results : The results of in vivo wound closure analysis revealed that CPNP treatments significantly improved wound contraction rates (p<0.01) at a faster rate than other three treatment groups. H&E staining revealed that CPNP treatments resulted in complete epithelialization and thick granulation tissue formation, whereas control groups resulted in a lack of compact epithelialization and persistence of inflammatory cells within the wound sites. Quantitative real-time PCR analysis showed that treatment with CPNPs suppressed IL-6 and TNF-α mRNA expression, and up-regulated TGF-β, VEGF-A and IL-10 mRNA expression. Western blot analysis showed up-regulated protein expression of TGF-β, VEGF-A and phosphorylatedSTAT3. Conclusion: Our results showed that CPNPs enhanced wound healing in DTI models, through modulation of the JAK2/STAT3 signalling pathway and subsequent upregulation of pro-healing factors.

Is the Success of Cefazolin plus Ertapenem in Methicillin-Susceptible Staphylococcus aureus Bacteremia Based on Release of Interleukin 1-beta?

2022 ◽  
Author(s):  
Dan Smelter ◽  
Mary Hayney ◽  
George Sakoulas ◽  
Warren Rose
Keyword(s):  
Staphylococcus Aureus ◽  
Peripheral Blood ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Blood Monocytes ◽  
Salvage Regimen ◽  
Peripheral Blood Monocytes ◽  
Staphylococcus Aureus Bacteremia

Cefazolin and ertapenem has been shown to be an effective salvage regimen for refractory methicillin-susceptible Staphylococcus aureus bacteremia. Our findings suggest cefazolin plus ertapenem in vitro stimulates interleukin-1β release from peripheral blood monocytes both with and without S. aureus presence. This IL-1β augmentation was primarily driven by ertapenem. These findings support further exploration of cefazolin plus ertapenem in MSSA bacteremia and may partially explain its marked potency in vivo despite modest synergy in vitro .

scholarly journals Association of Nicotine with Osteochondrogenesis and Osteoarthritis Development: The State of the Art of Preclinical Research

2019 ◽  
Vol 8 (10) ◽  
pp. 1699
Author(s):  
Xiaoyu Cai ◽  
Liang Gao ◽  
Magali Cucchiarini ◽  
Henning Madry
Keyword(s):  
Articular Chondrocytes ◽  
Clinical Effects ◽  
Nicotine Exposure ◽  
Protective Effects ◽  
Preclinical Research ◽  
Positive Effects ◽  
Osteochondral Repair ◽  
Dose Dependent

The deleterious effects of nicotine on various health conditions have been well documented. Although many orthopedic diseases are adversely affected by nicotine, little is known about its preclinical effects on chondrogenesis or osteogenesis, cartilage formation, osteoarthritis (OA), and osteochondral repair. A systematic review was conducted examining the current scientific evidence on the effects of nicotine on chondrogenesis or osteogenesis in vitro, possible consequences of prenatal nicotine exposure (PNE) on cartilage and OA susceptibility in the offspring, and whether nicotine affects OA development and osteochondral repair in vivo, always focusing on their underlying mechanisms. The data reveal dose-dependent effects on articular chondrocytes and on the chondrogenesis and osteogenesis of medicinal signaling cells in vitro, with lower doses often resulting in positive effects and higher doses causing negative effects. PNE negatively affects articular cartilage development and induces OA in the offspring without or with nicotine exposure. In contrast, protective effects on OA development were only reported in monosodium iodoacetate-induced small animal models. Finally, nicotine repressed MSC-based osteochondral repair in vivo. Future studies need to investigate dose-dependent clinical effects of smoking on cartilage quality in offspring, OA susceptibility and progression, and osteochondral repair more in detail, thus identifying possible thresholds for its pathological effects.

Aging and dietary modulation of elastase and interleukin-1 beta secretion

1995 ◽  
Vol 268 (1) ◽  
pp. R208-R213 ◽  
Author(s):  
J. G. Cannon ◽  
M. A. Fiatarone ◽  
M. Meydani ◽  
J. Gong ◽  
L. Scott ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Cell Function ◽  
Interleukin 1 ◽  
Lipid Peroxide ◽  
Arachidonic Acid Metabolism ◽  
Interleukin 1 Beta ◽  
Tension Development ◽  
Age Related

Aging is associated with diminished immune function that may stem from alterations in arachidonic acid metabolism and lipid peroxidation. This study sought to determine if dietary modification of fatty acids influenced neutrophil and monocyte secretion after an in vivo inflammatory stress in older human subjects. Volunteers participated in protocols that forced their quadriceps muscles to lengthen during tension development (eccentric stress). These protocols can cause inflammatory foci in the muscle as well as alterations in circulating leukocyte function. In this study, in vivo neutrophil degranulation was assessed by plasma elastase concentrations, and mononuclear cell function was assessed by interleukin-1 beta (IL-1 beta) secretion in vitro. In response to eccentric stress, older subjects (> 60 yr old) taking a placebo had no apparent elastase response, whereas those taking fish oil supplements responded with a 142% increase in plasma elastase (P = 0.011), similar to responses of younger reference subjects (< 33 yr old) taking no supplement. Overall, elastase responses correlated with individual plasma arachidonic acid-to-eicosapentaenoic acid ratios (r = -0.881, P = 0.004). Thus apparent age-related differences in elastase release were reconciled by individual differences in fatty acid nutriture. No significant temporal changes in urinary lipid peroxide excretion or IL-1 beta secretion were observed; however, age-associated differences were found.

Effect of fluoxetine on interleukin-1 beta in rat brain – in vivo and in vitro studies

2010 ◽  
Vol 62 ◽  
pp. 57
Author(s):  
Ewa Obuchowicz ◽  
Anna Bielecka ◽  
Agnieszka Prymus ◽  
Łukasz Drzyzga ◽  
Monika Paul-Samojedny ◽  
...  
Keyword(s):  
Rat Brain ◽  
Interleukin 1 ◽  
In Vitro Studies ◽  
Interleukin 1 Beta

scholarly journals Specnvezhenide Decreases Interleukin-1β-Induced Inflammation on Rat Chondrocytes via NF-κB and wnt/β-Catenin Pathways and Reduces Joint Destruction in Osteoarthritic Rats

2017 ◽  
Author(s):  
Chiyuan Ma ◽  
Jisheng Ran ◽  
Kai Xu ◽  
Langhai Xu ◽  
Yute Yang ◽  
...  
Keyword(s):  
Subchondral Bone ◽  
Therapeutic Potential ◽  
Interleukin 1 ◽  
Joint Destruction ◽  
Beta Catenin ◽  
Interleukin 1 Beta ◽  
Nf Kappa B ◽  
Inflammatory Effect

As a chronic disease, osteoarthritis (OA) leads to degradation of both cartilage and subchondral bone, of which the development is related to proinflammatory cytokines like interleukin-1&beta;. In the present study, the anti-inflammatory effect of Specnvezhenide in osteoarthritis and mechanism of it was studied in vitro and in vivo. The results showed that Specnvezhenide decreases interleukin-1&beta;-induced expression of matix-degrading enzymes and reduces the activation of NF-&kappa;B and wnt/&beta;-catenin pathways in vitro. Furthermore, Specnvezhenide treatment prevents the degeneration of both cartilage and subchondral bone in rats OA model. As conclusion, to the best of our knowledge, we report firstly that Specnvezhenide decreases interleukin-1&beta;-induced inflammation on rat chondrocytes by inhibiting activation of NF-&kappa;B and wnt/&beta;-catenin pathways, and has therapeutic potential in OA treatment.

scholarly journals Omeprazole increases survival via different mechanisms in two rat models of liver injury

2021 ◽  
Author(s):  
Masaya Kotsuka ◽  
Yuki Hashimoto ◽  
Richi Nakatake ◽  
Tetsuya Okuyama ◽  
Masahiko Hatta ◽  
...  
Keyword(s):  
Liver Injury ◽  
Mrna Expression ◽  
Rat Hepatocytes ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Beneficial Effects ◽  
Factor Alpha ◽  
Oxide Synthase

Abstract Omeprazole (OMZ) is a proton pump inhibitor (PPI) that is used to reduce gastric acid secretion, but little is known about its possible liver protective effects. This study investigated whether OMZ has beneficial effects in rat septic models of lipopolysaccharide (LPS)-induced liver injury after D-galactosamine (GalN) treatment and 70% hepatectomy (PH), and to determine the mechanisms of OMZ in an in vitro model of liver injury. In the in vivo models, the effects of OMZ were examined 1 h before treatment. OMZ increased survival and decreased tumor necrosis factor-alpha, inducible nitric oxide synthase, cytokine-induced neutrophil chemoattractant 1, interleukin (IL)-6, and IL-1β mRNA expression, and increased IL-10 mRNA expression in the livers of both GaIN/LPS- and PH/LPS-treated rats. Necrosis and apoptosis were inhibited by OMZ in GaIN/LPS rats, but OMZ had no effects on necrosis in PH/LPS rats. Primary rat hepatocytes were treated with IL1-β in the presence or absence of OMZ (in vitro model). OMZ inhibited iNOS induction partially through suppression of NF-κB signaling in hepatocytes. Furthermore, OMZ inhibited the induction of several inflammatory mediators, resulting in the prevention of LPS-induced liver injury after GalN liver failure and PH, although OMZ showed different doses and mechanisms in the two models.

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