Search results for: Mouse Anti-Influenza-B
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Home alone: a systematic review and meta-analysis on the effects of individual housing on body weight, food intake and visceral fat mass in rodents.Rats and mice are widely used to study environmental effects on psychological and metabolic health. Study designs differ widely and are often characterized by varying (social) housing conditions. In itself, housing has a profound influence on physiology and behaviour of rodents, affecting energy balance and sustainable metabolic health. However, evidence for potential long-term consequences of individual versus social housing on body weight and metabolic phenotype is inconsistent. We conducted a systematic literature review and meta-analyses assessing effects of individual versus social housing of rats and mice, living under well-accepted laboratory conditions, on measures of metabolic health, including body weight, food intake and visceral adipose tissue mass. Seventy-one studies were included in this review; 59 were included in the meta-analysis. Whilst housing did not affect body weight, both food intake and visceral adipose tissue mass were significantly higher in individually compared with socially housed animals. A combination of emotional stress and lack of social thermoregulation likely contributed to these effects. Increased awareness of consequences and improved specifications of housing conditions are necessary to accurately evaluate efficacy of drugs, diets or other interventions on metabolic and other health outcomes because housing conditions are rarely considered as possible moderators of reported outcomes.
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Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy.Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1-/-) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1-/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1-/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1-/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1-/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1-/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1.
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Anti-obesity effects of Clausena excavata in high-fat diet-induced obese mice.Clausena excavata (C. excavata) has been used as a traditional medicine for the treatment of abdominal pain, enteritis, dysentery, and malaria. The present study was designed to evaluate the effect of a 50% ethanol extract of C. excavata (ECE) on weight loss, adipocyte size, and obesity-related biochemical parameters in high-fat diet (HFD)-induced obese mice. After 6 weeks of HFD + ECE administration, HFD-induced total fat, subcutaneous fat, and visceral fat were evaluated by micro-computed tomography. The serum levels of triglyceride (TG), total cholesterol (TCH), high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein (LDL) cholesterol were evaluated with a biochemical analyzer, and leptin and adiponectin levels in the serum were assessed via enzyme-linked immunoassay (ELISA). Moreover, adipocyte size and lipid formation in the liver were examined. We found that weight gain, epididymal fat pad weight, adipocyte size, and lipid formation were markedly attenuated in the livers of HFD-induced obese mice treated with ECE. Furthermore, TG, TCH, and leptin decreased in the serum, whereas adiponectin increased. In conclusion, our data show that ECE has potent anti-obesity activity in vivo and support the development of ECE as a potential therapeutic agent for the treatment of obesity.
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Lidanpaidu prescription alleviates lipopolysaccharide-induced acute kidney injury by suppressing the NF-κB signaling pathway.The Lidanpaidu Prescription (LDP), a hospital preparation, composed of Chinese classical preparations, has been reported to have antiendotoxin, anticoagulant and other effects. However, its therapeutic effect on lipopolysaccharide (LPS)-induced acute kidney injury (AKI) and the mechanisms remain unclear. Therefore, we administered LPD pretreatment at different doses to examine the protective effects and mechanisms in LPS-induced AKI in mice. The kidney injury induced by LPS was assessed by histological examination. ELISA was used to detect the levels of inflammatory cytokines. The mRNA expression of the inflammatory genes IKKβ and TNF-α in kidney tissues was assessed by RT-PCR. Finally, Western blot was performed to assess the NF-κB signaling pathway related proteins, and the nuclear translocation of NF-kB P65 was detected by immunofluorescence laser confocal microscopy. The findings suggested that LDP significantly improved at 48 h animal survival (66.7%), compared with the LPS group (26.7%), determined by a Kaplan-Meier analysis. LDP attenuated the kidney histopathological changes induced by LPS and decreased the inflammatory cytokine levels in serum and renal tissue. Moreover, LDP markedly inhibited the expression of inflammatory genes and suppressed the activation of relevant proteins in the nucleus. In summary, these findings suggest that LDP reduces LPS-induced AKI via a mechanism related to the suppression of the NF-κB signaling pathway.
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Methyl dehydroabietate counters high fat diet-induced insulin resistance and hepatic steatosis by modulating peroxisome proliferator-activated receptor signaling in mice.The aim of this study was to investigate the therapeutic effects of methyl dehydroabietate (mDA) on adipocyte differentiation in 3T3-L1 preadipocytes and obesity characteristics induced by high-fat diet (HFD) in mice. Adipocyte differentiation in 3T3-L1 cells was evaluated after 14 days of incubation with mDA. mDA enhanced adipocyte differentiation in 3T3-L1 cells. For the in vivo evaluation, five-week-old male C57BL/6J mice were fed HFD or normal CE-2 diet (control) for eight weeks. During the experimental period, mice were administered mDA (50 mg/kg, p.o.) as an olive oil emulsion (containing 10% ethanol), and body weights were measured weekly. At the end of the experiment, the mice were euthanized after 16 h fasting period, and plasma samples were collected. The liver, kidney, and epididymal adipose tissues were collected and weighed. It significantly decreased body weight, adipose tissue weight, and plasma levels of glucose, insulin, leptin, and pro-inflammatory cytokines compared with that in the HFD group, and markedly reduced the impairment in glucose tolerance in obese mice. Furthermore, mDA reduced HFD-induced adipocyte hypertrophy and the formation of hepatic lipid droplets. Moreover, it induced the expression of proliferator-activated receptor alpha (PPARα) in the liver and PPARγ in the adipose tissues. Our findings demonstrate that mDA reduces obesity-induced glucose and insulin tolerance by inducing PPAR expression.
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Effects of perinatal fluoride exposure on the expressions of miR-124 and miR-132 in hippocampus of mouse pups.To investigate the effects of perinatal fluoride exposure on learning and memory ability of mouse offspring, ICR female mice were received different doses of sodium fluoride (0, 25, 50, 100 mg/L NaF) from pregnant day 7 to lactational day 21. Pups were exposed to fluoride through the cord blood and breast milk. Open field test showed that compared to the control group, perinatal fluoride exposure significantly decreased the number of entries into the center zone in 100 mg/L NaF group. In the eight-arm maze test, the number of working memory errors, reference memory errors, and the total arm entries were significantly increased in fluoride treatment groups, compared to the control group. Additionally, 100 mg/L NaF significantly elevated the expression levels of miR-124, miR-132, and DiGeorge syndrome chromosomal region 8 (DGCR8) in hippocampus of mouse pups at postnatal day (PND) 21. Contrarily, methyl CpG binding protein 2 (MeCP2) were dramatically reduced in 50 and 100 mg/L NaF groups, while cAMP-response element binding protein (CREB) mRNA level was significantly decreased in all fluoride groups. These findings suggested that the impairment of learning and memory in mouse offspring induced by perinatal fluoride exposure may partly result from the enhanced miR-124 and miR-132 and the alterations of their target genes.
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High-Dose Metformin Plus Temozolomide Shows Increased Anti-tumor Effects in Glioblastoma In Vitro and In Vivo Compared with Monotherapy.The purpose of the study is to investigate the efficacy of combined treatment with temozolomide (TMZ) and metformin for glioblastoma (GBM) in vitro and in vivo.
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Highly Dispersible and Bioavailable Curcumin but not Native Curcumin Induces Brown-Like Adipocyte Formation in Mice.The induction of brown-like adipocytes in white adipose tissue (WAT) is a potential therapeutic target for the treatment of obesity and metabolic disorders via the ability of these cells to release excess energy as heat in association with uncoupling protein 1. Some experimental trials suggest that curcumin (a yellow pigment from turmeric) has a suppressive effect on the accumulation of body fat. However, there is little evidence to show that curcumin induces the formation of brown-like adipocytes and the molecular mechanisms involved remain elusive. In addition, in most experimental trials, high doses of curcumin are administered.
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In vitro and in vivo metabolite identification of a novel benzimidazole compound ZLN005 by LC-MS/MS.A novel benzimidazole compound ZLN005 was previously identified as a transcriptional activator of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) in certain metabolic tissues. Upregulation of PGC-1α by ZLN005 has been shown to have beneficial effect in a diabetic mouse model and in a coronary artery disease model in vitro. ZLN005 could also have therapeutic potential in neurodegenerative diseases involving down-regulation of PGC-1α. Given the phenotypic efficacy of ZLN005 in several animal models of human disease, its metabolic profile was investigated to guide the development of novel therapeutics using ZLN005 as the lead compound.
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Improved Long-term Volume Retention of SVF-gel Grafting with Enhanced Angiogenesis and Adipogenesis.The apoptosis of mature adipocytes after fat grafting can result in chronic inflammation, absorption, and fibrosis, leading to unpredictable outcomes. Selective elimination of mature adipocytes may result in better outcomes and a different underlying retention mode. We previously developed a mature-adipocyte-free product, SVF-gel, derived from lipoaspirate, which eliminates adipocytes while preserving the stromal vascular fraction. This study investigated the retention and regeneration mode of SVF-gel grafting.
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