Search results for: JNK1
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Electroacupuncture Attenuates Morphine Tolerance in Rats with Bone Cancer Pain by Inhibiting PI3K/Akt/JNK1/2 Signaling Pathway in the Spinal Dorsal Horn.
Morphine is often used for the treatment of moderate and severe cancer pain, but long-term use can lead to morphine tolerance. Methods for effectively inhibiting morphine tolerance and the related mechanism of action are of great significance for the treatment of cancer pain. Previous studies have shown that electroacupuncture (EA) can inhibit the occurrence of morphine tolerance, but the mechanism is not yet clear. The aim of the present study was to explore the signaling pathway by which EA attenuates the development of bone cancer pain (BCP)-morphine tolerance (MT).Bin Jiang, Xuemei Zhong, Junfan Fang, Aijun Zhang, Wen WangD, Yi Liang, Jianqiao Fang, Feng Chen, Junying Du
1811 related Products with: Electroacupuncture Attenuates Morphine Tolerance in Rats with Bone Cancer Pain by Inhibiting PI3K/Akt/JNK1/2 Signaling Pathway in the Spinal Dorsal Horn.
2 Pieces/BoxInhibitors5mg2 Pieces/Box2 Pieces/Box8 inhibitors2 Pieces/Box2 Pieces/Box14 inhibitors
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#33641906 2021/01/27
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Mesoporous silica coated carbon nanofibers reduce embryotoxicity via ERK and JNK pathways.
Carbon nanofibers (CNFs) have been implicated in biomedical applications, yet, they are still considered as a potential hazard. Conversely, mesoporous silica is a biocompatible compound that has been used in various biomedical applications. In this regard, we recently reported that CNFs induce significant toxicity on the early stage of embryogenesis in addition to the inhibition of its angiogenesis. Thus, we herein use mesoporous silica coating of CNFs (MCNFs) in order to explore their outcome on normal development and angiogenesis using avian embryos at 3 days and its chorioallantoic membrane (CAM) at 6 days of incubation. Our data show that mesoporous silica coating of CNFs significantly reduces embryotoxicity provoked by CNFs. However, MCNFs exhibit slight increase in angiogenesis inhibition in comparison with CNFs. Further investigation revealed that MCNFs slightly deregulate the expression patterns of key controller genes involved in cell proliferation, survival, angiogenesis, and apoptosis as compared to CNFs. We confirmed these data using avian primary normal embryonic fibroblast cells established in our lab. Regarding the molecular pathways, we found that MCNFs downregulate the expression of ERK1/ERK2, p-ERK1/ERK2 and JNK1/JNK2/JNK3, thus indicating a protective role of MCNFs via ERK and JNK pathways. Our data suggest that coating CNFs with a layer of mesoporous silica can overcome their toxicity making them suitable for use in biomedical applications. Nevertheless, further investigations are required to evaluate the effects of MCNFs and their mechanisms using different in vitro and in vivo models.Ghada G Abdo, Ishita Gupta, Hadeel Kheraldine, Balsam Rizeq, Moustafa M Zagho, Ashraf Khalil, Ahmed Elzatahry, Ala-Eddin Al Moustafa
1843 related Products with: Mesoporous silica coated carbon nanofibers reduce embryotoxicity via ERK and JNK pathways.
2 gbox
100 slides1000pcs 1 plate 1KG100 ug/vial250ul500 mg100ug5 g100μg/vial10
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#33632212 2021/02/04
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UTRN inhibits melanoma growth by suppressing p38 and JNK/c-Jun signaling pathways.
Utrophin (UTRN), as a tumor suppressor gene, is involved in various cancer progression. The function of UTRN in the melanoma process and the related molecular mechanisms are still unclear. Herein, we studied the function of UTRN in melanoma growth and the relevant molecular mechanisms.Sitong Zhou, Wen Ouyang, Xi Zhang, Lexi Liao, Xiaobing Pi, Ronghua Yang, Baiqiang Mei, Huaiyuan Xu, Shijian Xiang, Jiehua Li
1743 related Products with: UTRN inhibits melanoma growth by suppressing p38 and JNK/c-Jun signaling pathways.
2 Pieces/Box2ug1 kit(96 Wells) 6 ml Ready-to-use 100ug500 MG2 Pieces/Box0.1 mg100ug100.00 ug50 ug250ul
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#33615154 2020/12/30
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JNK1 ablation improves pancreatic β-cell mass and function in db/db diabetic mice without affecting insulin sensitivity and adipose tissue inflammation.
The cJun N-terminal Kinases (JNK) emerged as a major link between obesity and insulin resistance, but their role in the loss of pancreatic β-cell mass and function driving the progression from insulin resistance to type-2 diabetes and in the complications of diabetes was not investigated to the same extent. Furthermore, it was shown that pan-JNK inhibition exacerbates kidney damage in the db/db model of obesity-driven diabetes. Here we investigate the role of JNK1 in the db/db model of obesity-driven type-2 diabetes. Mice with systemic ablation of JNK1 (JNK1) were backcrossed for more than 10 generations in db/+ C57BL/KS mice to generate db/db-JNK1 mice and db/db control mice. To define the role of JNK1 in the loss of β-cell mass and function occurring during obesity-driven diabetes we performed comprehensive metabolic phenotyping, evaluated steatosis and metabolic inflammation, performed morphometric and cellular composition analysis of pancreatic islets, and evaluated kidney function in db/db-JNK1 mice and db/db controls. db/db-JNK1 mice and db/db control mice developed insulin resistance, fatty liver, and metabolic inflammation to a similar extent. However, db/db-JNK1 mice displayed better glucose tolerance and improved insulin levels during glucose tolerance test, higher pancreatic insulin content, and larger pancreatic islets with more β-cells than db/db mice. Finally, albuminuria, kidney histopathology, kidney inflammation and oxidative stress in db/db-JNK1 mice and in db/db mice were similar. Our data indicate that selective JNK1 ablation improves glucose tolerance in db/db mice by reducing the loss of functional β-cells occurring in the db/db mouse model of obesity-driven diabetes, without significantly affecting metabolic inflammation, steatosis, and insulin sensitivity. Furthermore, we have found that, differently from what previously reported for pan-JNK inhibitors, selective JNK1 ablation does not exacerbate kidney dysfunction in db/db mice. We conclude that selective JNK1 inactivation may have a superior therapeutic index than pan-JNK inhibition in obesity-driven diabetes.Arianna Mazzoli, Claudia Sardi, Ludovic Breasson, Franziska Theilig, Barbara Becattini, Giovanni Solinas
1572 related Products with: JNK1 ablation improves pancreatic β-cell mass and function in db/db diabetic mice without affecting insulin sensitivity and adipose tissue inflammation.
96 assays
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#33613525 2021/02/05
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JNK1 Signaling Downstream of the EGFR Pathway Contributes to Aldara-Induced Skin Inflammation.
c-Jun N-terminal protein kinase 1 (JNK1) is involved in multiple biological processes but its implication in inflammatory skin diseases is still poorly defined. Herein, we studied the role of JNK1 in the context of Aldara-induced skin inflammation. We observed that constitutive ablation of JNK1 reduced Aldara-induced acanthosis and expression of inflammatory markers. Conditional deletion of JNK1 in myeloid cells led to reduced skin inflammation, a finding that was associated with impaired Aldara-induced inflammasome activation . Next, we evaluated the specific role of JNK1 in epidermal cells. We observed reduced Aldara-induced acanthosis despite similar levels of inflammatory markers. Transcriptomic and epigenomic analysis of keratinocytes revealed the potential involvement of JNK1 in the EGFR signaling pathway. Finally, we show that inhibition of the EGFR pathway reduced Aldara-induced acanthosis. Taken together, these data indicate that JNK1 plays a dual role in the context of psoriasis by regulating the production of inflammatory cytokines by myeloid cells and the sensitivity of keratinocytes to EGFR ligands. These results suggest that JNK1 could represent a valuable therapeutic target in the context of psoriasis.Aurore Le, Abdulkader Azouz, Séverine Thomas, Nicolas Istaces, Muriel Nguyen, Stanislas Goriely
1607 related Products with: JNK1 Signaling Downstream of the EGFR Pathway Contributes to Aldara-Induced Skin Inflammation.
14 inhibitors2 Pieces/BoxOne 96-Well Strip Micropl2 Pieces/Box1 mg1.5 x 10^6 cells7 inhibitors2 Pieces/BoxOne 96-Well Strip Micropl2 Pieces/Box
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#33607044 2021/02/16
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JNK1 signaling in the proximal tubule causes cell death and acute renal failure in rat and mouse models of renal ischaemia/reperfusion injury.
Activation of the JUN amino-terminal kinase (JNK) pathway is prominent in most forms of acute and progressive tubulointerstitial damage, including acute renal ischaemia/reperfusion injury (IRI). There are two forms of JNK expressed in the kidney, JNK1 and JNK2. Systemic administration of pan-JNK inhibitors suppress renal IRI; however, the contribution of JNK1 versus JNK2, and the specific role of JNK activation in the proximal tubule in IRI remains unknown. These questions were addressed in rat and mouse models of acute bilateral renal IRI. Administration of the JNK inhibitor, CC-930, substantially reduced the severity of renal failure, tubular damage and inflammation at 24hr in a rat IRI model. Next, Jnk1-/- mice, but not Jnk2-/- mice, were shown to be significantly protected against acute renal failure, tubular damage and inflammation in the IRI model. Furthermore, mice with conditional Jnk1 deletion in the proximal tubule also showed considerable protection from IRI-induced renal failure, tubular damage and inflammation. Finally, primary cultures of Jnk1-/-, but not Jnk2-/-, tubular epithelial cells were protected from oxidant-induced cell death, in association with preventing phosphorylation of proteins (RIP3 and MLKL) in the necroptosis pathway. In conclusion, JNK1 but not JNK2 plays a specific role in IRI-induced cell death in the proximal tubule leading to acute renal failure.Keren Grynberg, Elyce Ozols, William R Mulley, Roger J Davis, Richard A Flavell, David J Nikolic-Paterson, Frank Y Ma
1778 related Products with: JNK1 signaling in the proximal tubule causes cell death and acute renal failure in rat and mouse models of renal ischaemia/reperfusion injury.
100 μg100 μg100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized2 Pieces/Box100ug Lyophilized100ug Lyophilized100ug Lyophilized
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#33602262 2021/02/18
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Differential and paradoxical roles of new-generation antidepressants in primary astrocytic inflammation.
Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are commonly used new-generation drugs for depression. Depressive symptoms are thought to be closely related to neuroinflammation. In this study, we used up-to-date protocols of culture and stimulation and aimed to understand how astrocytes respond to the antidepressants.Jia-Hui He, Rong-Pei Liu, Yi-Man Peng, Qing Guo, Lan-Bing Zhu, Yi-Zhi Lian, Bei-Lei Hu, Hui-Hui Fan, Xiong Zhang, Jian-Hong Zhu
1398 related Products with: Differential and paradoxical roles of new-generation antidepressants in primary astrocytic inflammation.
4 Membranes/Box8 Sample Kit16 Arrays/Slide16-22 Sample Kit8 Sample Kit4 Arrays/Slide4 Sample Kit16 Arrays/Slide8 Sample Kit1-8 Sample Kit4 Sample Kit
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#33601292 2021/02/15
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Modulation of the inflammatory environment by spermatozoa through regulation of transforming growth factor beta in porcine uterine epithelial cells.
This study investigated the changes in the mRNA expression of transforming growth factor beta (TGF-β), plasminogen activators (PAs), and interleukin (IL) caused by sperm, as well as the regulatory mechanism of PA activity through TGF-β, in porcine uterine epithelial cells. The cells were isolated from the uterine horn of pig and co-incubated with Percoll-separated boar sperm (45% or 90%), or TGF-β for 24 h. The mRNA expression of TGF-β isoforms (TGF-β1, 2 and 3) and their receptors (TGF-β R1 and R2), PAs (urokinase-type, uPA; tissue-type, tPA; uPA receptor, uPAR; type 1 PA inhibitor, PAI-1), IL-6 and IL-8 was analyzed using real-time PCR. Supernatant was used to measure PA activity. Co-incubation with sperm from the 90% Percoll layer increased TGF-β1 mRNA, whereas TGF-β2 and TGF-β3 were decreased (P < 0.05). However, both TGF-βRs were not changed by the presence of the spermatozoa. Expression of tPA, PAI-1, IL-6, and IL-8 mRNA was down-regulated by 90% Percoll-separated sperm (P < 0.05), and sperm from 45% Percoll increased uPA expression (P < 0.05). TGF-β decreased tPA and IL-8 mRNA expression, and increased uPAR and PAI-1 mRNA (P < 0.05). The suppressive effect of TGF-β on PA activity was blocked by Smad2/3 and JNK1/2 signaling inhibitors (P < 0.05). In conclusion, sperm separated in 90% in porcine uterus could suppressed inflammation via modulation of TGF-β and down-regulation of PAs and ILs. Therefore, the regulatory mechanism of inflammation by sperm in the porcine uterus could be associated with interactions between numerous cytokines including TGF-β.Su-Jin Kim, Yong Hwangbo, Choon-Keun Park
1499 related Products with: Modulation of the inflammatory environment by spermatozoa through regulation of transforming growth factor beta in porcine uterine epithelial cells.
5 x 50 ug2ug1ug50 ug20ug96T96 wells100.00 ug10ugProtein10 ug
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#33600944 2021/02/15
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A novel strategy for glioblastoma treatment by induction of noptosis, an NQO1-dependent necrosis.
Glioblastoma (GBM) is one of the most prevalent malignant primary tumors in the human brain. Temozolomide (TMZ), the chemotherapeutic drug for GBM treatment, induces apoptosis. Unfortunately, apoptosis-resistance to TMZ results in treatment failure. GBM shows enhanced expression of NAD(P)H: quinone oxidoreductase 1 (NQO1). Recently, noptosis, a type of NQO1-dependent necrosis, was proposed. Here, we identified that tanshindiol B (TSB) inhibits GBM growth by induction of noptosis. TSB triggered significant cell death, which did not fit the criteria of apoptosis but oxidative stress-induced necrosis. Molecular docking, cellular thermal shift assay, and NQO1 activity assay revealed that TSB bind to and promptly activated NQO1 enzyme activity. As the substrate of NQO1, TSB induced oxidative stress, which resulted in dramatic DNA damage, poly (ADP-ribose) polymerase 1 (PARP1) hyperactivation, and NAD depletion, leading to necrotic cell death. These effects of TSB were completely abolished by specific NQO1 inhibitor dicoumarol (DIC). Furthermore, the c-Jun N-terminal kinase 1/2 (JNK1/2) plays an essential role in mediating TSB-induced cell death. Besides, TSB significantly suppressed tumor growth in a zebrafish xenograft model mediated by NQO1. In conclusion, these results showed that TSB was an NQO1 substrate and triggered noptosis of GBM. TSB exhibited anti-tumor potentials in GBM both in vitro and in vivo. This study provides a novel strategy for fighting GBM through the induction of noptosis.Bingling Zhong, Jie Yu, Ying Hou, Nana Ai, Wei Ge, Jin-Jian Lu, Xiuping Chen
1586 related Products with: A novel strategy for glioblastoma treatment by induction of noptosis, an NQO1-dependent necrosis.
100ug Lyophilized 100ul50 assays100ug Lyophilized100 20 100μg100 100ul100ug Lyophilized0.1 ml100ug Lyophilized
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#33595160 2021/02/17
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Expression of farnesyl pyrophosphate synthase is increased in diabetic cardiomyopathy.
Farnesyl pyrophosphate synthase (FPPS)-catalyzed isoprenoid intermediates are involved in diabetic cardiomyopathy. The present study investigated the specific role of FPPS in the development of diabetic cardiomyopathy. We demonstrated that FPPS expression was elevated in both in-vivo and in-vitro models of diabetic cardiomyopathy. FPPS inhibition decreased the expression of proteins related to cardiac fibrosis and cardiomyocytic hypertrophy, including collagen I, collagen III, connective tissue growth factor, natriuretic factor, brain natriuretic peptide, and β-myosin heavy chain. Furthermore, FPPS inhibition and knockdown prevented phosphorylated JNK1/2 activation in-vitro. In addition, a JNK1/2 inhibitor downregulated high-glucose-induced responses to diabetic cardiomyopathy. Finally, immunofluorescence revealed that cardiomyocytic size was elevated by high glucose and was decreased by zoledronate, siFPPS, and a JNK1/2 inhibitor. Taken together, our findings indicate that FPPS and JNK1/2 may be part of a signaling pathway that plays an important role in diabetic cardiomyopathy. This article is protected by copyright. All rights reserved.Zhengwei Li, Jiefang Zhang, Min Wang, Fuyu Qiu, Chongyin Jin, Guosheng Fu