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#32473615   2020/05/30 To Up

Display of quintuple glucagon-like peptide 1 (28-36) nonapeptide on Bacillus subtilis spore for oral administration in the treatment of type 2 diabetes.

To develop an oral delivery system of glucagon-like peptide 1 (GLP-1)(28-36) for treating Type-2 Diabetes, B.S-GLP-1(28-36), a recombinant Bacillus subtilis spores transformed with a plasmid vector encoding five consecutive GLP-1 (28-36) nonapeptides with an enterokinase site was constructed.
Mengna Kang, Fan Feng, Qi Ge, Feifei Zhu, Liang Chen, Peng Lv, Shangshang Ma, Qin Yao, Keping Chen

2642 related Products with: Display of quintuple glucagon-like peptide 1 (28-36) nonapeptide on Bacillus subtilis spore for oral administration in the treatment of type 2 diabetes.

200ul100μl100ug Lyophilized 5 G250 mg100ug Lyophilized96 assays250ul200ul50 ug100ug50 ug

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#32473614   2020/05/30 To Up

Potential dual functional roles of the Y-linked RBMY in hepatocarcinogenesis.

The hepatocellular carcinoma (HCC) is a highly heterogenous liver cancer with significant male-biases in incidence, disease progression and outcomes. Previous studies suggested that genes on the Y-chromosome could be expressed and exert various male-specific functions in the oncogenic processes. In particular, the RNA-binding motif on the Y chromosome (RBMY) gene is frequently activated in HCC and postulated to promote hepatic oncogenesis in patients and animal models. In the present study, immunohistochemical analyses of HCC specimens and datamining of TCGA database revealed that high-level RBMY expression is associated with poor prognosis and survival of the patients, suggesting that RBMY could possess oncogenic properties in HCC. To examine the immediate effect(s) of the RBMY overexpression in liver cancer cells, cell proliferation was analyzed on HuH-7 and HepG2 cells. The results unexpectedly showed that RBMY overexpression inhibits cell proliferation in both cell lines as its immediate effects, which lead to vast cell death in HuH-7 cells. Transcriptome analysis showed that genes involved in various cell proliferative pathways, such as the RAS/RAF/MAP and PIP3/AKT signaling pathways, were down-regulated by RBMY overexpression in HuH-7 cells. Further, in vivo analyses in a mouse liver cancer model using hydrodynamic tail vein injection of constitutively active AKT and RAS oncogenes showed that RBMY abolishes the HCC development. The findings support the notion that the Y-linked RBMY could serve dual tumor suppressing and promoting functions, depending on the spatiotemporal and magnitude of its expression during the oncogenic processes, thereby contributing to the sexual dimorphisms in liver cancer.
Tatsuo Kido, Z Laura Tabatabai, Xin Chen, Yun-Fai Chris Lau

1616 related Products with: Potential dual functional roles of the Y-linked RBMY in hepatocarcinogenesis.

1100 μg50 ul20 ul20 ul50 ul20 ul

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#32473608   2020/05/30 To Up

Protective effects of Coenzyme Q10 against sevoflurane-induced cognitive impairment through regulating apolipoprotein E and phosphorylated Tau expression in young mice.

Children with multiple exposures to anesthesia and surgery may be more likely to develop learning disability. Coenzyme Q10 (CoQ10) was reported to reduce the multiple sevoflurane treatment induced cognitive deficiency in 6-day old young mice. However, its specific mechanisms have not yet been found. This research aimed to reveal the role of ApoE in the pathogenesis of cognitive deficiency caused by sevoflurane anesthesia and the protective mechanism of CoQ10 in a multiple sevoflurane treatment model of young mice. The mice were randomly divided into 4 groups: Control + corn oil, Sevoflurane + corn oil, Control + CoQ10 and Sevoflurane + CoQ10. Sevoflurane group mice were anesthetized with 3% sevoflurane and 60% oxygen 2 hours a day for 3 days, while control group mice received only 60% oxygen. Mice received intraperitoneal injection of 50mg/kg CoQ10 or the same volume of corn oil 30 min before inhalation of oxygen or sevoflurane for 3 days. Mice received sevoflurane anesthesia or control treatment from the 6th to 8th day after birth. The cortex and hippocampus were harvested on the 8th day. The ATP, MMP, ApoE mRNA, total ApoE, ApoE fragments, Aβ1-40, Aβ1-42, Tau5, AT8 and PHF levels were detected. The Morris water maze (MWM) tests were performed from P30 to p36 after anesthesia or control treatment. The results indicated that the injection of CoQ10 ahead of sevoflurane treatment could reversed the anesthesia induced energy deficiency, mitochondrial dysfunction, ApoE and its fragments expression, Aβ1-42 generation, Tau phosphorylation and cognitive impairment in young mice. These data reveal that the ApoE and its fragments enhancement may play an important role in the pathogenesis of cognitive deficiency caused by sevoflurane anesthesia. CoQ10 could reduce ApoE expression by improving energy replenishment and mitochondrial functions, thereby alleviating sevoflurane-induced brain damage and cognitive impairment.
Man Yang, Hong Tan, Kai Zhang, Naqi Lian, Yang Yu, Yonghao Yu

1884 related Products with: Protective effects of Coenzyme Q10 against sevoflurane-induced cognitive impairment through regulating apolipoprotein E and phosphorylated Tau expression in young mice.

5ug2ug300 units96 assays400 ug96T400 ug1 mg1 mg96 wells (1 kit)96T

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#32473572   2020/05/27 To Up

The improvement effect of gastrodin on LPS/GalN-induced fulminant hepatitis via inhibiting inflammation and apoptosis and restoring autophagy.

Fulminant hepatitis (FH), characterized by overwhelmed inflammation and massive hepatocyte apoptosis, is a life-threatening and high mortality rate. Gastrodin (GTD), a phenolic glucoside extracted from Gastrodiaelata Blume, exerts anti-apoptosis, and anti-inflammatory activities. In the present study, we aimed to evaluate whether GTD treatment could alleviate lipopolysaccharide and d-galactosamine (LPS/GalN)-induced FH in mice and its potential mechanisms. These data suggested that GTD treatment remarkably protected against LPS/GalN-induced FH by enhancing the survival rate of mice, reducing ALT and AST levels, attenuating histopathological changes, and suppressing interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α secretion. In addition, GTD treatment relieved hepatic apoptosis by the regulation of peroxisome proliferator-activated receptors (PPARs), P53 and caspase-3/9. Furthermore, GTD treatment could significantly inhibit inflammation-related signaling pathways activated by LPS/GalN, including the suppression of nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) and nuclear factor-kappa B (NF-κB) activation. Importantly, GTD treatment effectively restored but not induced LPS/GalN-reduced the expression of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) phosphorylation, as well as the level of pro-autophagy proteins. Taken together, our investigation indicated that GTD played an essential role in liver protection by relieving hepatocyte apoptosis and inflammation reaction, which may be closely involved in the inhibition of NLRP3 inflammasome and NF-κB activation, regulation of apoptosis-related proteins expression, and the recovery of AMPK/ACC/autophagy.
Hongming Lv, Yuanyuan Liu, Boxi Zhang, Yuwei Zheng, Hong Ji, Shize Li

2803 related Products with: The improvement effect of gastrodin on LPS/GalN-induced fulminant hepatitis via inhibiting inflammation and apoptosis and restoring autophagy.

100 mg 25 MG25 mg200ug1000 10 mg100ug1000 tests200ul25 mg100 mg

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#32473571   2020/05/27 To Up

PIK3R3 regulates ZO-1 expression through the NF-kB pathway in inflammatory bowel disease.

Inflammatory bowel disease (IBD) are the major risk factor for developing colitis associated cancer (CAC). Previously, we have reported that Phosphoinositide-3-kinase regulatory subunit 3 (PIK3R3) was overexpressed in colorectal cancer (CRC), but we don't know the role of PIK3R3 in IBD.
Sidikjan Ibrahim, Xu Zhu, Xuelai Luo, Yongdong Feng, Jing Wang

2491 related Products with: PIK3R3 regulates ZO-1 expression through the NF-kB pathway in inflammatory bowel disease.

100ug100ug Lyophilized100ug Lyophilized100ug Lyophilized1000 100ug10ug100ug Lyophilized2 Pieces/Box100ug Lyophilized5 g

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#32473570   2020/05/27 To Up

Recombinant human ulinastatin improves immune dysfunction of dendritic cells in septic mice by inhibiting endoplasmic reticulum stress-related apoptosis.

Urinary trypsin inhibitor (UTI), also known as ulinastatin, has been reported to protect multiple organs against inflammation- and/or injury-induced dysfunction. In the present study, we aimed to investigate the immunomodulation effects of a recombinant human ulinastatin (urinary trypsin inhibitor, UTI) (rhUTI) on splenic dendritic cells (DCs) in cecal ligation and puncture (CLP)-induced septic mice. CLP mice were treated with rhUTI intramuscularly at 0, 12, and 24 h after procedure. Splenic CD11c DCs were isolated and accessed with flow cytometry for apoptotic or phenotypic analysis. Protein markers and cytokines were determined with Western blotting or ELISA. Treatment with rhUTI could markedly upregulate levels of costimulatory molecules (CD80, CD86) and MHC-II on surface of the splenic DC in CLP mice. The apoptotic rate of splenic DCs was decreased in CLP mice after rhUTI treatment. The survival rate of septic mice was increased after treatment with rhUTI. In addition, protein level of markers in endoplasmic reticulum stress (ERS)-related apoptotic pathways (including GRP78, caspase-12, and CHOP) were obviously down-regulated in the rhUTI-treated group when compared with the CLP group. These results indicate that rhUTI protects CLP-induced sepsis in mice by improving immune response of splenic DCs and inhibiting the excessive ERS-mediated apoptosis.
An-Long Qi, Yao Wu, Ning Dong, Yan-Fen Chai, Xiao-Mei Zhu, Yong-Ming Yao

1766 related Products with: Recombinant human ulinastatin improves immune dysfunction of dendritic cells in septic mice by inhibiting endoplasmic reticulum stress-related apoptosis.

1 mg10 ug 100ul100 ug10 25 100 UG10 25 mg5 2 10

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#32473533   2020/05/22 To Up

Polarization and function of tumor-associated macrophages mediate graphene oxide-induced photothermal cancer therapy.

Polarization status of tumor-associated macrophages (TAMs) plays an essential role in tumor growth and invasion. However, emerging treatment like photothermal therapy (PTT), photodynamic therapy (PDT) paid little attention on TAMs. In recent years, photothermal therapy (PTT) has gained immense attention in the anti-tumor strategy field while the effect of PTT on macrophage polarization in a tumor microenvironment has rarely been reported. Here, we used graphene oxide (GO) combined with polyethylene glycol (PEG) as the photothermal material to induce heating effect in macrophages to define its anti-tumor effect in vitro and in vivo. Firstly, we treated the macrophage cell line RAW264.7 with near infrared (NIR) light irradiation and detected their polarization status by flow cytometric and mRNA expression analysis. Following this, we analyzed the migration and invasion ability of an osteosarcoma HOS cell line cultured in a conditioned medium (CM) that contains cytokine generated by macrophages with or without NIR treatment. Finally, we investigated the in vivo effects of NIR-induced macrophage polarization on osteosarcoma growth and invasion. GO-PEG (GP) showed great photothermal effect, thermal stability, and biocompatibility in vitro and in vivo. Photothermal materials can alleviate interleukin-4-induced M2 polarization of macrophages and modulate their anti-tumor capability. Thus, the migration and invasion capabilities of HOS cells were weakened, leading to an anti-tumor effect in a mouse subcutaneous tumor model. In conclusion, our study identified PTT treatment as an approach for preventing osteosarcoma invasion by inhibition of M2 polarization.
Xiangyu Deng, Hang Liang, Wenbo Yang, Zengwu Shao

1861 related Products with: Polarization and function of tumor-associated macrophages mediate graphene oxide-induced photothermal cancer therapy.

200 TESTS 100 G

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#32473405   2020/05/27 To Up

STAT5 is required for lipid breakdown and beta-adrenergic responsiveness of brown adipose tissue.

Increasing energy expenditure through activation of brown adipose tissue (BAT) thermogenesis is an attractive approach to counteract obesity. Thus, it is essential to understand the molecular mechanisms that control BAT functions. Until now several members of the Janus kinase (JAK) - signal transducer and activator of transcription (STAT) pathway have been implicated to be relevant for BAT physiology. Yet, whether the STAT family member STAT5 is important for the thermogenic property of adipose tissues is unknown. Here, we investigate the role of STAT5 in thermogenic fat.
Doris Kaltenecker, Katrin Spirk, Frank Ruge, Florian Grebien, Marco Herling, Anne Rupprecht, Lukas Kenner, Elena E Pohl, Kristina M Mueller, Richard Moriggl

2345 related Products with: STAT5 is required for lipid breakdown and beta-adrenergic responsiveness of brown adipose tissue.

0.1 ml0.1ml (1mg/ml)100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized25 μg100ug Lyophilized100ug Lyophilized100ug Lyophilized

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#32473376   2020/05/27 To Up

SP-D Loaded PLGA Nanoparticles as Drug Delivery System for Prevention and Treatment of Premature Infant's Lung Diseases.

Preterm infants, particularly those who born between 23 and 28 weeks' gestation, suffer from a very high incidence of respiratory distress syndrome (RDS) related to pulmonary immaturity and inability to make Pulmonary Surfactant (PS). These infants are supported by the use of oxygen, ventilators, and routine administration of surfactant replacement. The currently commercial surfactant replacement therapies do not contain hydrophilic surfactant proteins such as Surfactant Protein D (SP-D). These proteins have a key role in the innate lung host defense, thus the development of a sustained release vehicle that provides SP-D for long periods in preterm infants' lungs would exploit the therapeutic potential of SP-D and other pulmonary medications. The proposed SP-D delivery system is based on nanoparticles (NPs) composed of poly (lactic acid-co-glycolic acid) (PLGA), a biodegradable, FDA approved biopolymer. The resulted NPs were spherical with high Zeta potential value, were not toxic to A-549 lungs cells, and did not induce any inflammatory response in mouse's lungs for short and long-term periods. Moreover, SP-D released from NPs showed biological activity for several days and in vivo release experiment of SP-D loaded NPs revealed that SP-D was released from NPs in mouse lungs with different NPs delivery doses.
Shani Attias Cohen, Paul S Kingma, J A Whitsett, Riki Goldbart, Tamar Traitel, Joseph Kost

2116 related Products with: SP-D Loaded PLGA Nanoparticles as Drug Delivery System for Prevention and Treatment of Premature Infant's Lung Diseases.

100 assays100 assays100 assays1,000 tests100 assays100 assays100 assays100 assays

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#32473368   2020/05/27 To Up

Dingkun pill replenishes diminished ovarian reserve through protection of primordial follicle pool by modulating the PI3K/AKT/mTOR signaling pathway.

Diminished ovarian reserve (DOR) can lead to poor fertility and shorten the reproductive lifespan of female. The Dingkun Pill (DKP), a traditional Chinese-patented medication has been an integral part of Chinese treatment for centuries for the management of gynecological diseases. Relevant clinical studies have shown that DKP is able to protect against DOR, however, its mechanism of action is not yet fully known.
Kun Ma, Yanxia Chen, Xiaodi Fan, Yuan Yuan, Kaili Wang, Caidie Tian, Min Li

2475 related Products with: Dingkun pill replenishes diminished ovarian reserve through protection of primordial follicle pool by modulating the PI3K/AKT/mTOR signaling pathway.

2 Pieces/Box1.5 x 10^6 cells5mg2 Pieces/Box5mgInhibitors2 Pieces/Box2 Pieces/Box5mg2 Pieces/Box1.5x10(6) cells50mg

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