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#32744344   2020/08/03 To Up

Protective effect of Lycium barbarum polysaccharide on ethanol-induced injury in human hepatocyte and its mechanism.

The purpose of this research is to study the effect of Lycium barbarum polysaccharide on ethanol-induced liver injury and its mechanism. The cell survival rate, the apoptosis rate, and the intracellular ROS level was detected by MTT assay, flow cytometry, laser confocal microscopy, and fluorescence spectrophotometry, respectively. The antioxidative indices were determined by ELISA kits and the protein level was detected by western blot. The result showed Lycium barbarum polysaccharide could protect ethanol-induced cell injury by reducing cell apoptosis and regulating the levels of indicators related to oxidative stress, such as ROS, MDA, SOD, etc. In addition, LBP could increase the nuclear expression of Nrf2 protein and significantly up-regulate the expression levels of Nrf2 protein and its downstream proteins, such as HO-1, NQO1, and GCLC in the cell nucleus. Therefore, Lycium barbarum polysaccharide has a protective effect on ethanol-induced liver cell injury and it plays the role in cell apoptosis pathway and oxidative stress pathway. PRACTICAL APPLICATIONS: Lycium barbarum is a kind of food that can be used as food and medicine in China. The result showed that Lycium barbarum polysaccharide could protect ethanol-induced liver cell injury, which is beneficial to the application of LBP in functional food.
Jianteng Wei, Linghao Zhang, Jianfei Liu, Dong Pei, Ningli Wang, Han Wang, Duolong Di, Yewei Liu

2143 related Products with: Protective effect of Lycium barbarum polysaccharide on ethanol-induced injury in human hepatocyte and its mechanism.

100ul100 ul5ug96T50 ul100 μg500 100 μg100 μg4 Membranes/Box100ug Lyophilized100 μg

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#32741111   2020/08/02 To Up

Canine atopic dermatitis: Role of luteolin as new natural treatment.

Luteolin has been demonstrated to possess numerous biological effects. However, the effect of luteolin on LPS (Lipopolysaccharides) stimulation in CPEK cells has not been investigated.
Enrico Gugliandolo, Ernesto Palma, Marika Cordaro, Ramona D'Amico, Alessio Filippo Peritore, Patrizia Licata, Rosalia Crupi

2739 related Products with: Canine atopic dermatitis: Role of luteolin as new natural treatment.

1ml1ml100 reactions100100 assays200 assays100 assays

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#32729158   2020/07/29 To Up

Propofol induces oxidative stress and apoptosis in vitro via regulating miR-363-3p/CREB signalling axis.

Propofol, a generally used anaesthetic in patients care, has been proven to induce neurotoxicity. Studies have shown that miR-363-3p was closely related to neurological dysfunction, and the up-regulated miR-363-3p was recognized to be participate in propofol-induced neurotoxicity. However, the mechanisms and functions of miR-363-3p in propofol-induced neurotoxicity remain rarely reported. The aim of our research was to clarify the potential effects of miR-363-3p in neurotoxicity induced by propofol. SH-SY5Y cells were treated with propofol, miR-363-3p inhibitor or sh-CREB. quantitative real-time polymerase chain reaction and western blotting were applied to detect the expression of miR-363-3p, CREB, Bax, Bcl-2, cleaved caspase-9 and cleaved caspase-3 at the mRNA and/or protein level, respectively. The levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) in cell supernatant were detected using different kits. Flow cytometry and MTT assay were applied for assessing the functions of miR-363-3p and CREB on cell ability in cellular activity and apoptotic rate. In addition, Bioinformatic analysis and luciferase assay verified the relationship between 3'-UTR of CREB and miR-363-3p. Our data indicated that the cell viability decreased with the increasing propofol concentration. Bioinformatic analysis and luciferase assay suggested that 3'-UTR of transcript of CREB might be a binding site of miR-363-3p, and miR-363-3p could negatively regulate the expression of CREB. The changes in reactive oxygen species, LDH, SOD and MDA suggested that propofol mediates oxidative stress and apoptosis via modulating miR-363-3p/CREB axis. Propofol induces oxidative stress and apoptosis via affecting miR-363-3p/CREB axis in SH-SY5Y cells, suggesting miR-363-3p down-regulation may act as a novel strategy to ameliorate the propofol-induced neurotoxicity. Significance of the study: The present study demonstrated that propofol induces oxidative stress and apoptosis via affecting miR-363-3p/CREB axis in SH-SY5Y cells, suggesting miR-363-3p down-regulation may act as a novel strategy to ameliorate the propofol-induced neurotoxicity.
Yi Yao, Jia-Jia Zhang

1597 related Products with: Propofol induces oxidative stress and apoptosis in vitro via regulating miR-363-3p/CREB signalling axis.

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#32720790   2020/07/27 To Up

6-Gingerol protects cardiomyocytes against hypoxia-induced injury by regulating the KCNQ1OT1/miR-340-5p/ PI3K/AKT pathway.

Hypoxia could induce cardiomyocytes injury and lead to heart disease. Studies have shown that 6-Gingerol has a protective effect on cardiomyocytes injury, but its molecular mechanism is still unclear.
Fan Pan, Xiaopeng Xu, Zhi Zhan, Qunfeng Xu

1813 related Products with: 6-Gingerol protects cardiomyocytes against hypoxia-induced injury by regulating the KCNQ1OT1/miR-340-5p/ PI3K/AKT pathway.

1 Set50mg100ug250ul100 IU1 Set2 Pieces/Box200ul2ug0.1 mg

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#32714095   2020/07/23 To Up

Circular RNA ITCH suppresses proliferation, invasion, and glycolysis of ovarian cancer cells by up-regulating CDH1 via sponging miR-106a.

Accumulating data suggested that circular RNAs (circRNAs) played important roles in the development of human cancer. However, the potential mechanism of circRNAs in ovarian cancer remains unclear.
Chunli Lin, Xiaofeng Xu, Qiumin Yang, Lu Liang, Shulin Qiao

2623 related Products with: Circular RNA ITCH suppresses proliferation, invasion, and glycolysis of ovarian cancer cells by up-regulating CDH1 via sponging miR-106a.

6 ml Ready-to-use 100 ug/vial50 ug100ìl x 10 vials

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#32705203   2020/07/09 To Up

DUSP6 protects murine podocytes from high glucose‑induced inflammation and apoptosis.

Diabetic nephropathy (DN) is one of the most severe complications that can occur in patients with diabetes, and without effective and timely therapeutic intervention, can gradually progress to renal failure. Previous studies have focused on investigating the pathogenesis of DN; however, the role of dual‑specificity phosphatase 6 (DUSP6) in DN is not completely understood. Therefore, the present study aimed to investigate the role of dual‑specificity phosphatase 6 (DUSP6) in DN. DN model mice were established and the expression levels of DUSP6 in the kidney tissues and high glucose (HG)‑induced murine podocytes (MPC5 cells) were determined using immunohistochemistry, reverse transcription‑quantitative PCR and western blotting. In addition, the levels of reactive oxygen species (ROS) and inflammatory cytokines in MPC5 cells were analyzed using commercial assay kits or ELISA kits, respectively, and flow cytometric analysis was performed to analyze the rate of cell apoptosis. The present study indicated that DUSP6 expression levels were significantly decreased in DN model mice compared with control mice, and in HG‑induced MPC5 cells compared with normal glucose‑induced MPC5 cells. DUSP6 overexpression enhanced MPC5 cell viability and increased protein expression levels of cell markers, such as synaptopodin and nephrin, compared with the negative control group. DUSP6 overexpression also reduced the levels of ROS and inflammatory cytokines, including interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α secreted by MPC5 cells under HG conditions. Moreover, compared with the HG group, cell apoptosis was inhibited by DUSP6 overexpression under HG conditions, which was further indicated by decreased expression levels of cleaved caspase‑3 and Bax. Thus, these findings indicated that DUSP6 mediated the protection against HG‑induced inflammatory response.
Liqiang Chen, Yaokun Wang, Haiyan Luan, Guangyu Ma, Huiming Zhang, Guang Chen

1494 related Products with: DUSP6 protects murine podocytes from high glucose‑induced inflammation and apoptosis.

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#32705172   2020/06/26 To Up

Vitamin D protects against necrotising enterocolitis in newborn mice by activating the ERK signalling pathway.

Necrotising enterocolitis (NEC) is a serious intestinal disease that occurs in the neonatal period. The present study aimed to investigate the protective effect of vitamin D on NEC and the underlying mechanisms. Artificial feeding and hypoxia‑cold stimulation were used to establish a mouse NEC model. IEC‑6 cells were treated with lipopolysaccharide (LPS) to establish the in vitro NEC model. Changes in the levels of interleukin (IL)‑6, IL‑1β and tumour necrosis factor (TNF)‑α, and activities of malondialdehyde (MDA) and glutathione peroxidase (GPx) were investigated via ELISA kits. In addition, mRNA expression of IL‑6, IL‑1β and TNF‑α and protein expression of phosphorylated (p)‑ERK1/2, Ki67, cleaved caspase‑3 and Bcl‑2 in intestinal tissues were determined via reverse transcription‑quantitative PCR and western blotting. Cell proliferation and apoptosis were also analysed via MTT assay and flow cytometry. In NEC mice, vitamin D reduced intestinal tissue damage, decreased the mRNA expression of IL‑6, IL‑1β and TNF‑α, and decreased the protein expression of cleaved caspase‑3 and MDA. Whereas, vitamin D increased the protein expression of Bcl‑2 and Ki67 and GPx, as well as the p‑ERK1/2/ERK1/2 ratio, in NEC mice. Furthermore, vitamin D improved cell viability, increased the ratio of p‑ERK1/2/ERK1/2, inhibited apoptosis, and decreased the mRNA expression of IL‑6, IL‑1β and TNF‑α in LPS‑treated IEC‑6 cells. The dual‑specificity mitogen‑activated protein kinase kinase inhibitor PD98059 reversed the effects of vitamin D on the proliferation, apoptosis and inflammation of LPS‑treated IEC‑6 cells. Overall, vitamin D relieved NEC in mice. Vitamin D promoted proliferation, and inhibited apoptosis and inflammation of LPS‑treated IEC‑6 cells by activating the ERK signalling pathway.
Chunmei Lyu, Suhua Jiang, Muxian Kong, Xiaoqian Chen, Li Zhang

1315 related Products with: Vitamin D protects against necrotising enterocolitis in newborn mice by activating the ERK signalling pathway.

Inhibitors100 μg100 μg20 ul

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#32685505   2020/06/23 To Up

Oltipraz Prevents High Glucose-Induced Oxidative Stress and Apoptosis in RSC96 Cells through the Nrf2/NQO1 Signalling Pathway.

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus (DM). Schwann cell (SC) apoptosis contributes to the occurrence and development of DPN. Effective drugs to prevent SC apoptosis are required to relieve and reverse peripheral nerve injury caused by DM. Oltipraz [4-methyl-5-(2-pyrazinyl)-1,2-dithiole-3-thione], an agonist of nuclear factor erythroid derived-2-related factor 2 (Nrf2), exerts strong effect against oxidative stress in animal models or clinical patients in certain diseases, including heart failure, acute kidney injury, and liver injury. The aim of the present study was to determine the effectiveness of oltipraz in preventing SC apoptosis induced by high glucose levels. RSC96 cells pretreated with oltipraz were cultured in high-glucose medium (50 mM glucose) for 24 h, and cells cultured in medium containing 5 mM glucose were used as the control. Flow cytometry was used to evaluate the degree of apoptosis. A Cell Counting Kit-8 assay was used to assess cell viability. The mitochondrial membrane potential was assessed using JC-1 staining, and reactive oxygen species (ROS) generation was measured using 20,70-dichlorodihydrofluorescein diacetate staining. In addition, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) levels were also evaluated using the corresponding kits. Flow cytometry was subsequently used to detect apoptosis, and western blotting was used to measure the expression levels of nuclear factor erythroid derived-2-related factor 2 and NADPH quinone oxidoreductase 1. The results showed that high glucose concentration increased oxidative stress and apoptosis in RSC96 cells. Oltipraz improved cell viability and reduced apoptosis of RSC96 cells in the high glucose environment. Additionally, oltipraz exhibited a significant antioxidative effect, as shown by the decrease in MDA levels, increased SOD levels, and reduced ROS generation in RSC96 cells. The results of the present study suggest that oltipraz exhibits potential as an effective drug for treatment with DPN.
Zengxin Jiang, Mengxuan Bian, Jingping Wu, Defang Li, Lei Ding, Qingmin Zeng

2378 related Products with: Oltipraz Prevents High Glucose-Induced Oxidative Stress and Apoptosis in RSC96 Cells through the Nrf2/NQO1 Signalling Pathway.

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#32665906   2020/05/11 To Up

Activation of PPARγ Inhibits TLR4 Signal Transduction Pathway in Melanoma Cancer .

Although peroxisome proliferator-activated receptor γ (PPARγ) is known as a regulator of fatty acid storage, fat cell differentiation, glucose and lipid metabolism, recent studies show that PPARγ has anticancer effects. The mechanisms of PPARγ activation in melanoma cancer remain unclarified. Recently, increased TLR4 expression has been associated with the melanoma cancer progression. We investigated whether the anti-cancer effect of PPARγ is through regulating TLR4 signaling pathway. Mouse melanoma cells (B16F10) were treated in different groups: control, pioglitazone (1, 10, 100, 300 µmol/L), lipopolysaccharide (LPS) (5 µg/mL) and LPS + pioglitazone. In another experiment, they were treated with CLI-095 (1 μM), and after 1 hour pioglitazone was added and subsequently stimulated with LPS. MTT assay was performed to measure the cell viability . The expression of genes were evaluated by quantitative reverse transcription PCR (qRT-PCR) in different groups. The concentration of tumor necrosis factor alpha and Interleukin 1 beta in the cell culture medium were measured by enzyme-linked immunosorbent assay (ELISA) kits. We show that activation of PPARγ by its agonist, pioglitazone, reduces cell proliferation, , , mRNA expression, and tumor necrosis factor-alpha (TNF-α) production but not interleukin-1 β (IL-1β) in B16F10 LPS-stimulated cells . Moreover, treatment of B16F10 cells with TLR4 inhibitor prior treatment with pioglitazone indicate that the anticancer effects of pioglitazone on melanoma cells was dependent on TLR4. The results indicate that pioglitazone has a beneficial protective effect against melanoma by affecting the TLR4 signaling pathway.
Nasim Dana, Golnaz Vaseghi, Shaghayegh Haghjooy Javanmard

1515 related Products with: Activation of PPARγ Inhibits TLR4 Signal Transduction Pathway in Melanoma Cancer .

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