جستجوی مقالات مرتبط با کلیدواژه "endotoxemia" در نشریات گروه "پزشکی"

Sepsis induces brain dysfunction and there is still a requirement for an unemployed viable restorative approach. This study aimed to investigate the role of dasatinib in the modulation of proinflammatory mediators, attenuating neuroinflammatory response, and it's signaling pathway during endotoxemia.

Experimental approach: 

Twenty-four adult male Swiss-albino mice were randomized into four groups: sham (undergo laparotomy without cecal ligation and puncture, sepsis (laparotomy with cecal ligation and puncture), vehicle-dimethyl sulfoxide, dasatinib (20 mg/kg/day) intraperitoneally. Brain tissue used for assessment of interleukin (IL)-6, IL-1β, tumor necrosis factor-alpha (TNF-α), IL-10, Toll-like receptor 4 (TLR4), protein kinase B (AKT), phosphoinositide 3-kinases (PI3K), signal transducer and activator of transcription 3 (STAT3), and histopathological examination.

Brain tissue levels of TNF-α, IL-6, and IL1 β were higher in the sepsis group than in the sham and vehicle groups. The dasatinib group had considerably lower tissue levels of these markers and significantly higher tissue values of IL-10 than the sepsis and vehicle groups. The sham group had much lower tissue values of TLR4, AKT, STAT3, and PI3k than in sepsis and vehicle groups. Furthermore, tissue levels of these markers in the dasatinib group were considerably lower than those in the sepsis and vehicle groups. Histopathology demonstrated that dasatinib might considerably reduce brain damage and the intensity of neuroinflammation when compared to sepsis and vehicle groups that showed extensive brain inflammation and damage.

Conclusion and implication: 

Dasatinib attenuated endotoxemia-induced acute brain damage in mice via modulating effects on TLR4, PI3K, AKT, and STAT3 downstream signaling pathways.

This study was done to investigate the potential neuroprotective effect of ipragliflozin during endotoxemia in mice.
Materials &

Twenty-four adult male Swiss-albino mice aged 8-12 weeks (25-35g) were randomized into four equal groups (n=6): sham (laparotomy without cecal ligation and puncture (CLP), sepsis (laparotomy with CLP), vehicle (equivalent volume of DMSO before CLP), and ipragliflozin (3mg/kg/day, orally before CLP). Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-1β, toll-like receptor 4 (TLR4), and P-signal transducer and activator of transcription (STAT)-3 levels were assessed in the brain tissue and histological examination was done.

The tissue levels of TNF-α, IL-6, and IL-1B in the sham group were much lower than in the sepsis and vehicle groups. Furthermore, the ipragliflozin group had considerably lower tissue levels of TNF-α, IL-6, and IL-1B compared to the sepsis and vehicle groups. However, the sham group showed much lower tissue levels of TLR4 and STAT3 compared to the sepsis and vehicle groups. Also, the tissue levels of TLR4 and STAT3 in the ipragliflozin group were considerably lower than those in the sepsis and vehicle groups. Histopathology analysis demonstrated that ipragliflozin might considerably reduce brain damage compared to sepsis and vehicle groups that showed interstitial edema and included glial cells with pyknotic nuclei.

Ipragliflozin attenuates brain dysfunction during CLP-induced polymicrobial sepsis in male mice.

The present study aimed to examine the neuroprotective effects of semaglutide during endotoxemia and its role in modulating pro-inflammatory mediators.
Materials &

Twenty-four adult male Swiss albino mice, 8-12 weeks old, weighing 25-35g, were randomly divided into four equal groups (n=6), including sham (laparotomy without cecal ligation and puncture, sepsis (laparotomy with CLP), vehicle (equivalent volume of distilled water before CLP), and semaglutide (40µg/kg/day before CLP). The brain was used for tissue evaluation of TNF-α, IL-6, IL-1β, TLR4, and P-STAT3, as well as for histological examination.

The tissue levels of TNF-α, IL-6 and IL-1β in the sham group were significantly lower than the sepsis and vehicle groups (p<0.05). In the semaglutide group, tissue levels of TNF-α, IL-6, and IL-1β were significantly lower than the sepsis and vehicle groups (p<0.05). The tissue levels of TLR4 and STAT3 in the sham group were significantly lower than the sepsis and vehicle groups (p<0.05). Also, tissue levels of TLR4 and STAT3 in the semaglutide group were significantly lower than the sepsis and vehicle groups (p<0.05). Histopathologically, semaglutide considerably reduced brain damage compared to the sepsis and vehicle groups.

Semaglutide can reduce brain dysfunction during CLP-induced polymicrobial sepsis in male mice through its modulating effects on TLR4STAT3 downstream signaling pathways and subsequently reducing inflammatory cytokines TNF-α, IL-6, and IL-1β.

Endotoxemia is the most common condition in patients treated in critical care units. This study aimed to investigate if dulaglutide may help to protect the lungs during endotoxemia by modulating the inflammatory and oxidative stress pathways. This study is self-funded. All authors contributed to the costs.
Materials &

20 adult male Swiss-albino mice aged 9–12 weeks, weighted 25–35g, were randomized into four equal groups (n=5), sham group (laparotomy without Cecal Ligation and Puncture (CLP), CLP group (laparotomy with CLP), vehicle group (normal saline 2 weeks before CLP), and dulaglutide group (0.6mg/kg twice weekly S.C for 2 weeks before CLP). After 24 hrs of sepsis, lung tissue was harvested and used to assess IL-6, Interleukin-IL-1β, TNF-α, MIF, TLR4, and 8-isoPGF2α, as well as histological examination.

Lung tissue levels of IL-6, IL-1β, TNF-α, MIF, TLR4, and F2-isoprostane were significantly higher in the sepsis group compared to the sham group (p<0.05), while dulaglutide group showed significantly lower level in these inflammatory mediators and oxidative stress compared to sepsis group (p<0.05). Histologically, all mice in the sepsis group showed a significant lung tissue injury (p<0.05), but this injury was significantly reduced in the dulaglutide pre-treated group (p<0.05).

Dulaglutide can attenuate acute lung injury during CLP-induced endotoxemia in mice through its modulating effects on TLR4 and oxidative stress, downstream signaling pathways, and subsequently decreased lung tissue levels of pro-inflammatory mediators.

Recent evidence has shown underlying roles of gut dysbiosis and metabolic endotoxemia in obesity and its complications. Despite the large number of experimental and clinical researches performed on gut microbiota and obesity, no bibliometrics’ study has been conducted so far. We aimed to assess the trend of global scientific publications in the field of gut microbiota and obesity. The bibliometrics’ data from January 2000 to April 2017 were retrieved based on Scopus database. The analysis of the publication year, main source, citation, subject area, co-authorship network, and geographical distribution were carried out, accordingly. The data were analyzed using the Scopus analysis tools, SPSS version 15 and Visualizing Scientific Landscapes (VOS) viewer version 1.6.5. Out of 4384 documents that were identified, the United States published the highest number (28.2%), followed by China and United Kingdom. The number of publications showed an increasing trend over the years of which the most productive year was 2016. The leading subject area was medicine. Most of published scientific documents were original articles and the top source was “PLoS One”. The documents were cited totally 153576 times with average citations per article as 35.03, and h-index of 159. Top author in the co-authorship network assessment was “Wang J.” from China. This study could provide practical sources to researchers to find highly cited studies. Moreover, the study could pave the way for researchers to be engaged in studies which potentially lead to more publication in the field

Myocardial ischemia may coincide and interact with sepsis and inflammation. Our objective was to examine the effects of bacterial endotoxin on myocardial functions and cell injury during acute ischemia. Rabbits were pretreated with incremental doses of E. Coli lipopolysaccharide (LPS) or normal saline. Myocardial ischemia was induced by 50-minute occlusion of left anterior descending artery. S-TNFaR was additionally used to block the effects LPS. Ventricular contractility as it was measured by dp/dt during systole decreased from 2445± 1298 to 1422 ± 944 mmHg/s, P =. 019. Isovolumetric relaxation time as an index of diastolic function was prolonged from 50±18 ms to 102± 64 ms following ischemia. Pretreatment with low concentrations of LPS (<1 µg) had no effect on dp/dt, while at higher concentrations it suppressed both contractility and prolonged IVRT. Cell injury as measured by cardiac troponin I level increased to 15.1± 3.2 ng/dL following ischemia and continued to rise with higher doses of LPS. While blocking TNFa did not improve the myocardial contractility after ischemia, it eliminated additional deleterious effects of LPS. Lower doses of LPS had no deleterious effect on myocardial function, whereas higher doses of this endotoxin cause cardiac dysfunction and increased extent of injury.