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Search results for: Human Like Collagen Recombinant

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#38417368   2024/02/27 To Up

Diannexin alleviates myocardial ischemia-reperfusion injury by orchestrating cardiomyocyte oxidative damage, macrophage polarization and fibrotic process by TLR4-NF-kB-mediated inactivation of NLRP3 inflammasome.

Myocardial ischemia-reperfusion (I/R) injury is a pathogenic mechanism of myocardial infarction and heart failure, constituting a major health concern globally. Diannexin is a homodimer of recombinant human annexin V and elicits important roles in several I/R injuries. Nevertheless, its function in MI/R remains elusive. Here, Diannexin alleviated simulated I/R (SI/R)-induced cardiomyocyte death and oxidative injury by increasing cell viability and inhibiting cell apoptosis, ROS, lactate dehydrogenase, malondialdehyde production and anti-oxidative SOD activity. Diannexin inhibited SI/R-induced expression of fibrotic protein collagen I and collagen III. Furthermore, Diannexin suppressed LPS-induced macrophage polarization towards pro-inflammatory M1-like phenotype and enhanced IL-4-evoked anti-inflammatory M2 polarization. Concomitantly, Diannexin inhibited SI/R exposure-induced macrophage polarization to M1 subtypes. Importantly, conditioned medium (CM) from SI/R-stimulated macrophages evoked cardiomyocyte apoptosis, which was reversed when cells were co-cultured with CM from Diannexin-treated macrophages under SI/R conditions. Mechanically, the activation of TLR4/NF-κB/NLRP3 inflammasome signaling in SI/R-treated cells was mitigated by Diannexin. Reactivating this pathway antagonized the protective effects of Diannexin on SI/R-induced cardiomyocyte oxidative injury, fibrotic protein expression and macrophage polarization and M1 macrophage-induced apoptosis of cardiomyocytes. In vivo, Diannexin alleviated abnormal cardiac structure, dysfunction and collagen position in MI/R mice. Additionally, Diannexin reduced M1-polarized and elevated M2-polarized macrophages in heart tissues at five days post-MI/R. The activation of TLR4/NF-κB/NLRP3 inflammasome pathway in MI/R mice was attenuated after Diannexin administration. Together, Diannexin may alleviate the development of MI/R injury by directly regulating cardiomyocyte oxidative injury, fibrotic potential and indirectly affecting macrophage polarization-mediated cardiomyocyte apoptosis, indicating a promising therapeutic strategy for MI/R.
Lin Zhang, Songlin Zhao, Yaqi Wang

2739 related Products with: Diannexin alleviates myocardial ischemia-reperfusion injury by orchestrating cardiomyocyte oxidative damage, macrophage polarization and fibrotic process by TLR4-NF-kB-mediated inactivation of NLRP3 inflammasome.

10 mg100ug100 ug500 MG0.1 mg250ul25 mg25 10 ug2ug96T100ul

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#38366861   2024/02/17 To Up

Delayed treatment with erythropoietin attenuates renal fibrosis in mouse model of unilateral ureteral obstruction.

Erythropoietin (EPO) exerts tissue-protective effects on various organs including the kidney. However, the effects of EPO on established renal fibrosis remain unclear. In this study, we aimed to examine the therapeutic potential of EPO against established renal fibrosis.
Akihiro Nishida, Masashi Nishida, Tomoko Iehara

2362 related Products with: Delayed treatment with erythropoietin attenuates renal fibrosis in mouse model of unilateral ureteral obstruction.

100 μg100 μg1mg100ug Lyophilized100ug100.00 ug100.00 ug4 Membranes/Box0.1ml100 μg100 μg

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#38318187   2024/01/22 To Up

Soluble CD147 regulates endostatin via its effects on the activities of MMP-9 and secreted proteasome 20S.

During progression of rheumatoid arthritis (RA), angiogenesis provides oxygen and nutrients for the cells' increased metabolic demands and number. To turn on angiogenesis, pro-angiogenic factors must outweigh anti-angiogenic factors. We have previously shown that CD147/extracellular matrix metalloproteinase inducer (EMMPRIN) can induce the expression of the pro-angiogenic factors vascular endothelial growth factor (VEGF) and matrix metallopeptidase 9 (MMP-9) in a co-culture of the human HT1080 fibrosarcoma and U937 monocytic-like cell lines. However, whether CD147 influences anti-angiogenic factors was not known. We now show that relative to single cultures, the co-culture of these cells not only enhanced pro-angiogenic factors but also decreased the anti-angiogenic factors endostatin and thrombospondin-1 (Tsp-1), generally increasing the angiogenic potential as measured by a wound assay. Using anti-CD147 antibody, CD147 small interfering RNA (siRNA), and recombinant CD147, we demonstrate that CD147 hormetically regulates the generation of endostatin but has no effect on Tsp-1. Since endostatin is cleaved from collagen XVIII (Col18A), we applied different protease inhibitors and established that MMP-9 and proteasome 20S, but not cathepsins, are responsible for endostatin generation. MMP-9 and proteasome 20S collaborate to synergistically enhance endostatin generation, and in a non-cellular system, CD147 enhanced MMP-9 activity and hormetically regulated proteasome 20S activity. Serum samples obtained from RA patients and healthy controls mostly corroborated these findings, indicating clinical relevance. Cumulatively, these findings suggest that secreted CD147 mediates a possibly allosteric effect on MMP-9 and proteasome 20S activities and can serve as a switch that turns angiogenesis on or off, depending on its ambient concentrations in the microenvironment.
Maya M Rahat, Hala Sabtan, Elina Simanovich, Amir Haddad, Tal Gazitt, Joy Feld, Gleb Slobodin, Adi Kibari, Muna Elias, Devy Zisman, Michal A Rahat

1872 related Products with: Soluble CD147 regulates endostatin via its effects on the activities of MMP-9 and secreted proteasome 20S.

100 U96tests 25 MG96tests1 kg1 g 25 MG5 mg100ug Lyophilized100ug Lyophilized100

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#38287796   // To Up

SIRT6 Reduces Rheumatoid Arthritis Injury by Inhibiting MyD88-ERK Signaling Pathway.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by destruction of synovial joints, abnormal immune responses and chronic inflammatory manifestations, which seriously affects patients' well-being. We explored this study to ascertain the effect and mechanism of silent information regulator 6 (SIRT6) on RA.
Xiaolong Yu, Zihan Jin, Faisal Raza, Ping Zhang, Jiabiao Wu, Min Ren, Jiapeng Wang, Jing Xi

2818 related Products with: SIRT6 Reduces Rheumatoid Arthritis Injury by Inhibiting MyD88-ERK Signaling Pathway.

2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box1.5 x 10^6 cells2 Pieces/Box1 mg2 Pieces/BoxInhibitors2 Pieces/Box2 Pieces/Box

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#38245791   2024/01/20 To Up

Chalcone-derivative L6H21 attenuates the OVA-induced asthma by targeting MD2.

Asthma represents a significant global challenge that affects individuals across all age groups and imposes substantial social and economic burden. Due to heterogeneity of the disease, not all patients obtain benefit with current treatments. The objective of this study was to explore the impact of MD2 on the progression of asthma using L6H21, a novel MD2 inhibitor, to identify potential targets and drug candidates for asthma treatment. To establish an asthma-related murine model and evaluate the effects of L6H21, ovalbumin (OVA) was used to sensitize and challenge mice. Pathological changes were examined with various staining techniques, such as H&E staining, glycogen staining, and Masson staining. Inflammatory cell infiltration and excessive cytokine secretion were evaluated by analyzing BALF cell count, RT-PCR, and ELISA. The TLR4/MD2 complex formation, as well as the activation of the MAPK and NF-кB pathways, was examined using western blot and co-IP. Treatment with L6H21 demonstrated alleviation of increased airway resistance, lung tissue injury, inflammatory cell infiltration and excessive cytokine secretion triggered by OVA. In addition, it also ameliorated mucus production and collagen deposition. In the L6H21 treatment group, inhibition of MAPK and NF-кB activation was observed, along with the disruption of TLR4/MD2 complex formation, in contrast to the model group. Thus, L6H21 effectively reduced the formation of the MD2 and TLR4 complex induced by OVA in a dose-dependent manner. This reduction resulted in the attenuation of MAPKs/NF-κB activation, enhanced suppression of inflammatory factor secretion, reduced excessive recruitment of inflammatory cells, and ultimately mitigated airway damage. MD2 emerges as a crucial target for asthma treatment, and L6H21, as an MD2 inhibitor, shows promise as a potential drug candidate for the treatment of asthma.
Xiangting Ge, Tingting Xu, Meiyan Wang, Lijiao Gao, Yue Tang, Ningjie Zhang, Rui Zheng, Weimin Zeng, Gaozhi Chen, Bing Zhang, Yuanrong Dai, Yali Zhang

2725 related Products with: Chalcone-derivative L6H21 attenuates the OVA-induced asthma by targeting MD2.

100 IU50 ul0.1 mg1500 Units1 mg50ug1

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#38155595   2024/01/03 To Up

A recombinant signalling-selective activated protein C that lacks anticoagulant activity is efficacious and safe in cutaneous wound preclinical models.

Various preclinical and clinical studies have demonstrated the robust wound healing capacity of the natural anticoagulant activated protein C (APC). A bioengineered APC variant designated 3K3A-APC retains APC's cytoprotective cell signalling actions with <10% anticoagulant activity. This study was aimed to provide preclinical evidence that 3K3A-APC is efficacious and safe as a wound healing agent. 3K3A-APC, like wild-type APC, demonstrated positive effects on proliferation of human skin cells (keratinocytes, endothelial cells and fibroblasts). Similarly it also increased matrix metollaproteinase-2 activation in keratinocytes and fibroblasts. Topical 3K3A-APC treatment at 10 or 30 μg both accelerated mouse wound healing when culled on Day 11. And at 10 μg, it was superior to APC and had half the dermal wound gape compared to control. Further testing was conducted in excisional porcine wounds due to their congruence to human skin. Here, 3K3A-APC advanced macroscopic healing in a dose-dependent manner (100, 250 and 500 μg) when culled on Day 21. This was histologically corroborated by greater collagen maturity, suggesting more advanced remodelling. A non-interference arm of this study found no evidence that topical 3K3A-APC caused either any significant systemic side-effects or any significant leakage into the circulation. However the female pigs exhibited transient and mild local reactions after treatments in week three, which did not impact healing. Overall these preclinical studies support the hypothesis that 3K3A-APC merits future human wound studies.
Ruilong Zhao, Meilang Xue, Haiyan Lin, Margaret Smith, Helena Liang, Hartmut Weiler, John H Griffin, Christopher J Jackson

2592 related Products with: A recombinant signalling-selective activated protein C that lacks anticoagulant activity is efficacious and safe in cutaneous wound preclinical models.

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

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#38069268   2023/11/29 To Up

A New Bioactive Fibrin Formulation Provided Superior Cartilage Regeneration in a Caprine Model.

The effective and long-term treatment of cartilage defects is an unmet need among patients worldwide. In the past, several synthetic and natural biomaterials have been designed to support functional articular cartilage formation. However, they have mostly failed to enhance the terminal stage of chondrogenic differentiation, leading to scar tissue formation after the operation. Growth factors substantially regulate cartilage regeneration by acting on receptors to trigger intracellular signaling and cell recruitment for tissue regeneration. In this study, we investigated the effect of recombinant insulin-like growth factor 1 (rIGF-1), loaded in fibrin microbeads (FibIGF1), on cartilage regeneration. rIGF-1-loaded fibrin microbeads were injected into full-thickness cartilage defects in the knees of goats. The stability, integration, and quality of tissue repair were evaluated at 1 and 6 months by gross morphology, histology, and collagen type II staining. The in vivo results showed that compared to plain fibrin samples, particularly at 6 months, FibIGF1 improved the functional cartilage formation, confirmed through gross morphology, histology, and collagen type II immunostaining. FibIGF1 could be a promising candidate for cartilage repair in the clinic.
Elif Vardar, Hui Yin Nam, Ganesh Vythilingam, Han Ling Tan, Haryanti Azura Mohamad Wali, Eva-Maria Engelhardt, Tunku Kamarul, Pierre-Yves Zambelli, Eleftheria Samara

1266 related Products with: A New Bioactive Fibrin Formulation Provided Superior Cartilage Regeneration in a Caprine Model.

18 kgs100 μg1 Set200ul1 Set100ug

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#38049981   2024/02/15 To Up

Counteracting tryptophan metabolism alterations as a new therapeutic strategy for rheumatoid arthritis.

Alterations in tryptophan (Trp) metabolism have been reported in inflammatory diseases, including rheumatoid arthritis (RA). However, understanding whether these alterations participate in RA development and can be considered putative therapeutic targets remains undetermined.In this study, we combined quantitative Trp metabolomics in the serum from patients with RA and corrective administration of a recombinant enzyme in experimental arthritis to address this question.
David Moulin, Marie Millard, Mahdia Taïeb, Chloé Michaudel, Anne Aucouturier, Antoine Lefèvre, Luis G Bermúdez-Humarán, Philippe Langella, Youssouf Sereme, Kristell Wanherdrick, Preeti Gautam, Xavier Mariette, Philippe Dieudé, Jacques-Eric Gottenberg, Jean-Yves Jouzeau, David Skurnik, Patrick Emond, Denis Mulleman, Jérémie Sellam, Harry Sokol

2097 related Products with: Counteracting tryptophan metabolism alterations as a new therapeutic strategy for rheumatoid arthritis.

50 assays100Tests100 tests100 assays96 Tests1,000 tests2.5 mg1 kit

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#38029612   2023/11/19 To Up

RhoGDI3 at the trans-Golgi network participates in NLRP3 inflammasome activation, VSMC phenotypic modulation, and neointima formation.

The pathological roles and mechanisms of Rho-specific guanine nucleotide dissociation inhibitor 3 (RhoGDI3) in vascular smooth muscle cell (VSMC) phenotypic modulation and neointima formation are currently unknown. This study aimed to investigate how RhoGDI3 regulates the Nod-like receptor protein 3 (NLRP3) inflammasome in platelet-derived growth factor-BB (PDGF-BB)-induced neointima formation.
Jingwen Sun, Qingyu Zhu, Xiaoqiang Yu, Xiuying Liang, Haijing Guan, Heyan Zhao, Wenjuan Yao

1819 related Products with: RhoGDI3 at the trans-Golgi network participates in NLRP3 inflammasome activation, VSMC phenotypic modulation, and neointima formation.

0.1mg2.5 mg2 mg4 Membranes/Box100 µl (2 mM)2.5 mg100 μg100 μg100 1 Set

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#38019085   // To Up

Study on the Effect of Type III Recombinant Humanized Collagen on Human Vascular Endothelial Cells.

The effect and mechanism of type III recombinant humanized collagen (hCOLIII) on human vascular endothelial EA.hy926 cells at the cellular and molecular levels were investigated. The impact of hCOLIII on the proliferation of EA.hy926 cells was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromid assay, the effect of hCOLIII on cell migration was investigated by scratch assay, the impact of hCOLIII on cell cycle and apoptosis was detected by flow cytometry, the ability of hCOLIII to induce angiogenesis of EA.hy926 cells was evaluated by angiogenesis assay, and the effect of hCOLIII on vascular endothelial growth factor (VEGF) expression was detected by real-time reverse transcription-polymerase chain reaction analysis. The hCOLIII at concentrations of 0.5, 0.25, and 0.125 mg/mL all showed specific effects on the proliferation and migration of human vascular endothelial cells. It could also affect the cell cycle, increase the proliferation index, and increase the expression level of VEGF in human vascular endothelial cells. In the meantime, hCOLIII at the concentration of 0.5 mg/mL also showed a promoting effect on vessel formation. hCOLIII can potentially promote the endothelization process of blood vessels, mainly by affecting the proliferation, migration, and vascular-like structure of human endothelial cells. At the same time, hCOLIII can promote the expression of VEGF. This collagen demonstrated its potential as a raw material for cardiovascular implants.
Han Wang, Yonghao Xiao, Yuanguo Zhang, Zhu Meng, Chenyu Zhao, Fanshan Qiu, Chongchong Li, Zengguo Feng

2503 related Products with: Study on the Effect of Type III Recombinant Humanized Collagen on Human Vascular Endothelial Cells.

2 1 mg2ug x 2010 μg501.00 flask1.00 flask 100ul

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