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#32746497   2020/08/03 To Up

Modulation of NADPH oxidase and Nrf2/HO-1 pathway by vanillin in cisplatin-induced nephrotoxicity in rats.

To investigate the protective effect of vanillin in cisplatin (CP)-induced nephrotoxicity in rats and elucidate the role of nrf-2 and its downstream antioxidant molecules.
Nahla N Younis, Nehal M Elsherbiny, Mohamed A Shaheen, Mohamed M Elseweidy

1939 related Products with: Modulation of NADPH oxidase and Nrf2/HO-1 pathway by vanillin in cisplatin-induced nephrotoxicity in rats.

100ug100ug 100ul10ug2 Pieces/Box7 inhibitors100ug Lyophilized100ug100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

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#32746451   2020/08/03 To Up

Antipsychotics drug aripiprazole as a lead against breast cancer cell line (MCF-7) in vitro.

Breast cancer is the second leading cause of death among women globally. The existing treatment options for breast cancer are largely associated with severe toxicities, and lower efficacies. Therefore, there is an urgent need for the development of non-toxic effective drugs against breast cancer. For this purpose, drug repositioning strategy was used to evaluate the anti-cancer potential of a library of heterocyclic drugs. The major advantage of drug repurposing is that the pharmacokinetic, pharmacodynamic, and toxicity profiles of drugs are well documented. In the current study, we screened 97 drugs of different chemical classes, and among them aripiprazole, an antipsychotic drug, was found to be sufficiently active against breast cancer cell line MCF-7. Aripiprazole showed a cytotoxicity (IC50 = 12.1 ± 0.40 μM) to MCF-7 cells, comparable to the standard anticancer drug doxorubicin (IC50 = 1.25 ± 0.34 μM). Aripiprazole was also found to be active against other cancer cell lines, including MDA-MB-231 (IC50 = 19.83 ± 0.27 μM), AU565 (IC50 = 18.02 ± 0.44 μM), and BT-474 (IC50 = 36.42 ± 0.12 μM). Aripiprazole significantly inhibited the cell cycle progression at subG0G1 phase, and enhanced apoptosis in MCF-7 breast cancer cells. The drug was also able to significantly increase the nuclear condensation, and modulated the expression of certain genes involved in breast cancer, such as caspases 3, and 9, BAK-1, C-MYC, BCL2L1, BCL-10, and BCL-2. Further studies are needed to explore the effect of aripiprazole on intrinsic and extrinsic pathways of apoptosis in cancer cells.
Adnan Badran, Atia Tul-Wahab, Humaira Zafar, Nayab Mohammad, Rehan Imad, Mariam Ashfaq Khan, Elias Baydoun, M Iqbal Choudhary

1388 related Products with: Antipsychotics drug aripiprazole as a lead against breast cancer cell line (MCF-7) in vitro.

96 tests100 Plates100 assays100 assays24 tests

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#32745769   2020/07/31 To Up

The insect molting hormone 20-hydroxyecdysone protects dopaminergic neurons against MPTP-induced neurotoxicity in a mouse model of Parkinson's disease.

20-hydroxyecdysone (20E), a steroidal prohormone, is secreted from the prothoracic glands. While 20E has been shown to have neuroprotective effects in Parkinson's disease (PD) models in vitro, its effects have not yet been examined in vivo. We sought to assess the behavioral and mechanistic effects of 20E on MPTP-induced toxicity in mice. To this end, we used behavioral tests, stereological analyses of dopaminergic neurons by tyrosine hydroxylase immunohistochemistry, and assessments of apoptotic mechanisms, focusing on Nrf2 signaling through Western blotting and ELISA assays. A 20E treatment protected against MPTP-induced motor incoordination, postural imbalance, and bradykinesia, and significantly reduced dopaminergic neuronal loss in the substantia nigra pars compacta (SNpc) and the striatum (ST). It also attenuated dopamine deficiency in the ST, modulated levels of antioxidative enzymes superoxide dismutase, catalase, and glutathione in the SNpc, increased the Bcl-2/Bax ratio, and inhibited cytosolic cytochrome c release and caspase-9, -7, and -3 activity in the SNpc. These results indicated that 20E inhibited the apoptotic cascade. Furthermore, the attenuation of MPTP neurotoxicity was associated with inhibited cleaved-caspase signaling pathways, along with upregulated Nrf2 pathways in the SNpc, suggesting that 20E mitigates MPTP-induced neurotoxicity via mitochondria-mediated apoptosis by modulating anti-oxidative activities. Our results suggest that 20E can inhibit MPTP-induced behavioral and neurotoxic effects in mice. This lays the foundation for further research on 20E as a potential target for therapeutic use.
Hye-Sun Lim, Byeong Cheol Moon, Jun Lee, Goya Choi, Gunhyuk Park

1800 related Products with: The insect molting hormone 20-hydroxyecdysone protects dopaminergic neurons against MPTP-induced neurotoxicity in a mouse model of Parkinson's disease.

50ug 50 ul100 ul96 tests1 mg4 Membranes/Box96T100 μg

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#32745765   2020/07/31 To Up

Hypoxic preconditioning combined with curcumin promotes cell survival and mitochondrial quality of bone marrow mesenchymal stem cells, and accelerates cutaneous wound healing via PGC-1α/SIRT3/ HIF-1α signaling.

Restrained survival and function of relocated bone marrow mesenchymal stem cells (BMSCs) is a major impediment to BMSCs-mediated tissue repair. Accumulating evidences have indicated that hypoxic preconditioning of BMSCs could enhance BMSCs' adaptability after transplantation and thus improve their therapeutic properties. Curcumin, a natural dietary product, is known to exert profound protective effects on various cellular processes. Here we showed that mild hypoxic preconditioning combined with curcumin significantly increased cell survival, enriched more cells in G2/M and S phase, and improved mitochondrial function in BMSCs. Meanwhile, hypoxic preconditioning combined with curcumin altered mitochondrial cristae shape and strongly inhibited mitochondrial cytochrome c release, which consequently suppressed an apoptosis signal as revealed by reduced caspase-3 cleavage in BMSCs. Moreover, hypoxic preconditioning remarkably promoted mitochondrial quality via increasing mitochondrial fusion and elevating the activity of oxidative phosphorylation (OXPHOS) and mitochondrial complex Ⅰ enzyme in BMSCs, which were in accordance with the up-regulated expression of OPA1, PINK1 and Parkin. At the mechanistic level, the destabilization of HIF-1α and the up-regulated expression of PGC-1α and SIRT3 synergistically contributed to the protective effects of hypoxic preconditioning combined with curcumin in BMSCs. The proteasome inhibitor MG132 stabilized HIF-1a expression, but not PGC-1α or SIRT3, and dramatically restrained BMSCs survival under hypoxia combined with curcumin condition. MG132 also increased mitochondrial superoxide and intracellular hydrogen peroxide (HO) production and caspase-3 activation in hypoxia combined with curcumin-treated BMSCs. Furthermore, knockdown of SIRT3 and PGC-1α by RNAi both led to caspase-3 activation in BMSCs after hypoxia and curcumin treatment. Notably, SIRT3 RNAi suppressed OXPHOS activity, while PGC-1α RNAi triggered mitochondrial superoxide and intracellular HO production in hypoxia combined with curcumin-treated BMSCs. Finally, we showed that hypoxia combined with curcumin-treated BMSCs accelerated the cutaneous wound healing process in a mice wound model. Overall, this study suggests that hypoxic preconditioning combined with curcumin could serve as an attractive strategy for facilitating BMSCs-mediated tissue repair, and further sheds new light on the rich repertoire of PGC-1α/SIRT3/HIF-1α signaling involved in the regulation of mitochondrial quality and function for cellular adaption to hypoxia.
Xujie Wang, Kuo Shen, Jing Wang, Kaituo Liu, Gaofeng Wu, Yan Li, Liang Luo, Zhao Zheng, Dahai Hu

1743 related Products with: Hypoxic preconditioning combined with curcumin promotes cell survival and mitochondrial quality of bone marrow mesenchymal stem cells, and accelerates cutaneous wound healing via PGC-1α/SIRT3/ HIF-1α signaling.

5 x 10A5 cells/vial1 vial1 x 10^6 cells/vial10 ug1.5 x 10^6 cells24 wells24 wells24 wells1.5x10(6) cells100 ug/vial1One Vial: 5 X 10^6 Cells

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#32745469   2020/07/31 To Up

miR-188-5p inhibits apoptosis of neuronal cells during oxygen-glucose deprivation (OGD)-induced stroke by suppressing PTEN.

The miRNAs and mRNAs are found to play a crucial role in modulating different diseases including stroke, according to the recent evidence. The current study is aimed at assessing the functional role played by miR-188-5p in the regulation of cell apoptosis and viability in OGD-induced human neural cell line HNC. With the help of RT-qPCR, the authors determined miR-188-5p as well as its putative target PTEN among OGD-treated cells in different treatment times. The cell viability was assessed through CCK-8 assay while the cell transfection either upregulated or may have silenced the genes. Both Western Blot as well as RT-qPCR found the proliferation biomarkers such as Ki87 and PCNA in addition to apoptosis biomarkers such as caspase-8 and caspase-3. The luciferase activity was tracked by conducting luciferase assay. The researchers observed an elevation in the expression of miR-188-5p while the PTEN got downregulated in Human Neural Cell line HNC with increase in the time span. The expressions of miR-188-5p and PTEN got increased with increasing OGD treatment time while the Luciferase reassured the binding site. The cell viability was suppressed by the overexpression of miR-188-5p which further inhibited the apoptosis biomarkers too. Meanwhile, it was understood that the results could be reversed to some extent with the inhibition of PTEN. The study findings from in vitro investigations yielded promising results and provided excellent insights about the fundamental molecular mechanisms of miR-188-5p involved in stroke via PTEN. This could be considered as a potential therapeutic axis among stroke patients in the near future.
Lijing Li, Penghua Cui, Huimin Ge, Yanjing Shi, Xiaoguang Wu, Zhongfan Ruan

2924 related Products with: miR-188-5p inhibits apoptosis of neuronal cells during oxygen-glucose deprivation (OGD)-induced stroke by suppressing PTEN.

96 assays 1 kit(s) 4 Membranes/Box50ml75 x 50ul/Unit200 200 1mg1.00 flask100 assays100 µg

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#32745467   2020/07/31 To Up

Globular adiponectin antagonizes leptin-induced growth of cancer cells by modulating inflammasomes activation: Critical role of HO-1 signaling.

Accumulating evidence suggests that adipokines, a group of hormones secreted from adipose tissue, modulate tumor growth in a complicated manner. Among diverse adipokines, adiponectin exerts potent anti-tumor activities, whereas leptin exhibits pro-tumorigenic properties. Herein, we have examined the opposing effect of adiponectin on leptin-induced growth of cancer cells and investigated the underlying mechanisms, particularly in the context of inflammasomes activation, which plays a role in the growth of cancer cells. Globular adiponectin (gAcrp) significantly suppressed leptin-induced growth of human breast (MCF-7) and hepatic (HepG2) cancer cells by modulating both cell cycle and apoptosis. To elucidate the underlying mechanisms, we examined the modulatory effects of gAcrp and leptin on inflammasomes. Herein, we showed that gAcrp substantially abolished leptin-induced inflammasomes activation, as evidenced by suppression of IL-1β maturation, caspase-1 activation, and downregulation of inflammasomes components, including NLRP3 and ASC, in both MCF-7 and HepG2 cancer cells. Interestingly, suppression of inflammasomes activation by gAcrp was almost completely restored by blockade of heme oxygenase-1 (HO-1) signaling. In addition, suppressive effects of gAcrp on ROS production and NADPH oxidase activation, both of which critically contribute to leptin-induced inflammasomes activation, disappeared by inhibition of HO-1 signaling. Moreover, gAcrp downregulated estrogen receptor-α (ER-α) expression and blocked leptin-induced ER-α activation, which also plays an important role in inflammasomes activation. Finally, the opposing effects of gAcrp on leptin-induced inflammasomes activation and tumor growth were further confirmed in MCF-7 tumor xenografts. In summary, treatment with gAcrp prevents leptin-induced cancer cell growth by modulating inflammasome activation, which is mediated, at least in part, via HO-1 induction and modulation of ER-α signaling.
Pawan Kumar Raut, Pil-Hoon Park

1505 related Products with: Globular adiponectin antagonizes leptin-induced growth of cancer cells by modulating inflammasomes activation: Critical role of HO-1 signaling.

5 x 50 ug100ug50 ug100ug100μg100ug100ul1x10e7 cells100ug100ug1000 100

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#32745381   2020/08/03 To Up

miR-21-5p protects hippocampal neurons of epileptic rats via inhibiting STAT3 expression.

Epilepsy is a common chronic neurological disorder worldwide.
Xiaolei Zhang, Xianfeng Li, Bin Li, Chengfeng Sun, Peng Zhang

2501 related Products with: miR-21-5p protects hippocampal neurons of epileptic rats via inhibiting STAT3 expression.

250ul100ug/vial24 reactions 1 kit1000pcs100 ug/vial0.2ug/ul,20ul100μg/vial100ug/vial

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#32745124   2020/08/03 To Up

Effective inhibition of cancer cells by recombinant adenovirus expressing EGFR-targeting artificial microRNA and reversed-caspase-3.

The EGFR-targeting cancer therapies are commonly facing drug resistance, mostly due to mutations. Gene therapy with artificial microRNA targeting EGFR conserved sequence may avoid such problem. In this study, we constructed a recombinant adenovirus expressing EGFR-targeting artificial microRNA and active revCASP3 (Ad-EC), under the control of tumor-specific SLPI promoter, and evaluated its inhibitory effect on HEP-2 cancer cells both in vitro and in vivo. MTT assay showed that cell growth inhibition rate at 72h was 44.0% in Ad-EC group at MOI 50, while the rate was 7.7% in the control virus Ad-GFP group and 3.6% in Cetuximab (500 μg/ml) group respectively. Flow cytometry analysis revealed the late apoptotic cells rate was 36.1% in Ad-EC group, significantly higher than 6.5% of Ad-GFP group (p < 0.001). When Ad-EC (MOI 50) was combined with CDDP (0.25 μg/ml), late apoptotic cells rate increased to 61.2%, significantly higher than each monotherapy group (P < 0.001). The real-time xCELLigence system recorded an effective cell growth inhibition in Ad-EC and CDDP groups, and more enhanced effect in Ad-EC plus CDDP group. Western blot revealed that Ad-EC could inhibit the activation of AKT pathway and ERK1/2 pathway, while Cetuximab had the AKT pathway over-activated. In vivo experiments with HEP-2 xenograft in nude mice confirmed the tumor inhibition in Ad-EC, CDDP and Ad-EC plus CDDP groups compared with PBS group (P < 0.01). Collectively, these data support the effective inhibition of cancer cells by this novel gene therapy strategy.
Maoxiao Yan, Jia Chen, Hua Jiang, Yuqiong Xie, Chunchun Li, Lihong Chen, Beibei Yang, Jiang Cao

2102 related Products with: Effective inhibition of cancer cells by recombinant adenovirus expressing EGFR-targeting artificial microRNA and reversed-caspase-3.

25 units201.00 flask100100100 units1.00 flask25 units96T100 units100 units1.00 flask

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#32744980   2020/07/29 To Up

Epigenetic Evaluation of N-(2-hydroxyphenyl)-2-propylpentanamide, a Valproic Acid Aryl Derivative with activity against HeLa cells.

Valproic acid (VPA) is an HDAC inhibitor (HDACI) with anticancer activity, but it is hepatotoxic. N-(2-hydroxyphenyl)-2-propylpentanamide (o-OH-VPA) is a VPA aryl derivative designed in silico as a selective inhibitor of HDAC8 with biological properties against HeLa, rhabdomyosarcoma and breast cancer cell cultures.
Luna-Palencia Gabriela Rebeca, Correa-Basurto José, Trujillo-Ferrara José, Meraz-Ríos Marco Antonio, Vásquez-Moctezuma Ismael

2743 related Products with: Epigenetic Evaluation of N-(2-hydroxyphenyl)-2-propylpentanamide, a Valproic Acid Aryl Derivative with activity against HeLa cells.

200 mg5 g5 mg25 mg

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#32744955   2020/07/30 To Up

Discovery and investigation of 1-[4-(2-aminoethoxy)phenylcarbonyl]-3,5-bis-(benzylidene)-4-piperidones as candidate antineoplastic agents: Our last 15 years study.

This review outlines the discovery and development of a novel series of 1-[4-2-aminoethoxy)phenylcarbonyl]- 3,5-bis-(benzylidene)-4-piperidones 5-8 as potential drug candidates over the last 15 years in our laboratory. Many of these compounds demonstrate excellent cytotoxic properties and are often more potent than contemporary anticancer drugs. Two highly important features of many of these molecules are first, the greater tumour-selective toxicity and second, the ability of these molecules to act as modulators of multi-drug resistance. The modes of action of some of the potent compounds are by apoptosis induction, generation of reactive oxygen species, activation of certain caspases and affecting mitochondrial functions. These molecules also display promising antimalarial and antimycobacterial properties. In a short term toxicity study, these molecules are well tolerated in mice. Structure-activity relationships, and a drug delivery system along with pharmacokinetic studies and metabolic stability of these compounds have been presented. The positive characteristics associated the series 5-8 warrants their further evaluations as candidate antineoplastic drug candidates.
Mohammad Hossain, Carlos E Enci, Jonathan R Dimmock, Umashankar Das

1210 related Products with: Discovery and investigation of 1-[4-(2-aminoethoxy)phenylcarbonyl]-3,5-bis-(benzylidene)-4-piperidones as candidate antineoplastic agents: Our last 15 years study.

10 mg20 g10 mg625/1560 assays250ul6 inhibitors15ml1 g100 μl1 kit1 kit

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