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Search results for: Metalloproteinase13

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#34425229   2021/08/20 To Up

Colchicine protects against cartilage degeneration by inhibiting MMP13 expression via PLC-γ1 phosphorylation.

Low molecular weight compounds that reduce the expression of MMP13 at the mRNA level might serve as disease-modifying osteoarthritis (OA) drugs (DMOADs). The objective of this study was to identify a candidate DMOAD that targets MMP13 expression.
K Takeuchi, H Ogawa, N Kuramitsu, K Akaike, A Goto, H Aoki, A Lassar, Y Suehara, A Hara, K Matsumoto, H Akiyama

2570 related Products with: Colchicine protects against cartilage degeneration by inhibiting MMP13 expression via PLC-γ1 phosphorylation.

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#34172768   2021/06/25 To Up

Combination of retinoids and narrow-band ultraviolet B inhibits matrix metalloproteinase 13 expression in HaCaT keratinocytes and a mouse model of psoriasis.

Matrix metalloproteinase13 (MMP13) can be released by keratinocytes and fibroblasts and involved in the pathogenesis of skin disorders. Retinoic acid derivative drugs include tazarotene and acitretin. Tazarotene/acitretin and narrow-band ultraviolet B (NB-UVB) irradiation are common treatment options for psoriasis. However, their impact on MMP13 expression in the context of psoriasis has yet to be determined. The expression of MMP13 was analyzed in patients with psoriasis. The effects of tazarotene/acitretin and NB-UVB on MMP13 expression were also investigated in a mouse model of psoriasis. Human HaCaT keratinocytes were exposed to acitretin or NB-UVB and then assayed for cell proliferation and MMP13 expression levels. We showed that patients with psoriasis had increased levels of MMP13 protein in skin lesions and serum samples. Exposure to acitretin and NB-UVB irradiation alone or in combination led to reduction of cell proliferation and MMP13 expression in HaCaT cells. Consistently, tazarotene treatment or NB-UVB irradiation attenuated imiquimod-induced psoriasis-like dermatitis and decreased MMP13 expression in a mouse model. Based on these from HaCaT keratinocytes cells and animal experiments, we suggest that tazarotene/acitretin and NB-UVB irradiation can inhibit the expression of MMP13 in HaCaT keratinocytes and psoriasis mouse models. Blockade of MMP13 activity may have therapeutic potential in improving symptoms of psoriasis.
Chan Xi, Chuanxi Xiong, Huiping Wang, Yuanjun Liu, Suju Luo

1196 related Products with: Combination of retinoids and narrow-band ultraviolet B inhibits matrix metalloproteinase 13 expression in HaCaT keratinocytes and a mouse model of psoriasis.

100ug100.00 ug1.00 mg100ul1000 TESTS/0.65ml100ug Lyophilized200 100ug100 100.00 ug

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#33448319   2021/01/15 To Up

Dihydroartemisinin attenuates osteoarthritis by inhibiting abnormal bone remodeling and angiogenesis in subchondral bone.

The present study aimed to investigate whether dihydroartemisinin (DHA) alleviates osteoarthritis (OA) in a mouse model of OA. Ten‑week‑old female C57BL/6j mice were used to establish OA models by anterior cruciate ligament transection (ACLT) and ovariectomized (OVX). DHA was then used to treat the OA in the ACLT and OVX mice. Safranin O‑fast green staining and Osteoarthritis Research Society International (OARSI)‑modified Mankin scores were used to grade articular cartilage degeneration. Expression of metalloproteinase‑13 (MMP‑13) and vascular endothelial growth factor (VEGF) in the articular cartilage and leukemia inhibitory factor (LIF), sclerostin, and β‑catenin in the subchondral bone were analyzed by immunohistochemistry. Expression of RANKL and CD31 were detected by immunofluorescence. Micro‑computed tomography was used to ascertain alterations in the microarchitecture of the subchondral bone. The results demonstrated that DHA decreased MMP‑13 and VEGF expression in the articular cartilage. DHA decreased OARSI scores and reduced articular cartilage degeneration. In addition, DHA reduced abnormal subchondral bone remodeling, as demonstrated by a reduction in trabecular separation (Tb.Sp), increased bone volume fractions (BV/TV), as well as bone mineral densities (BMD) compared with the ACLT+vehicle group and the OVX+vehicle group. Furthermore, DHA decreased the inhibition of sclerostin through reduction of LIF secretion by osteoclasts and, hence, attenuated aberrant bone remodeling and inhibited angiogenesis in subchondral bone, further reducing the progression of OA. The present study demonstrated that DHA attenuated OA by inhibiting abnormal bone remodeling and angiogenesis in subchondral bone, which may be a potential therapeutic target for this disease.
Long Ma, Xin Zhao, Yibin Liu, Jiang Wu, Xiaochun Yang, Qunhua Jin

1753 related Products with: Dihydroartemisinin attenuates osteoarthritis by inhibiting abnormal bone remodeling and angiogenesis in subchondral bone.

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#32196852   2020/04/13 To Up

Andrographolide mitigates cartilage damage via miR-27-3p-modulated matrix metalloproteinase13 repression.

As a potential anti-arthritic agent, Andrographolide (And) is capable of promoting chondrocyte proliferation and preventing apoptosis in pathologic condition. The present study aimed to explore the roles of And in in vivo and in vitro models of osteoarthritis (OA), as well as its underlying molecular mechanisms.
Shaojian Chen, Zhihuan Luo, Xiaguang Chen

1950 related Products with: Andrographolide mitigates cartilage damage via miR-27-3p-modulated matrix metalloproteinase13 repression.

2 ml0.1 mg96 wells (1 kit)0.1 mg100 ug/vial0.1ml (1mg/ml)100|uI x 10 vialsN/A 100ug100 vial100 ug/vial

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#32073014   2020/02/19 To Up

Glycyrrhizin inhibits osteoarthritis development through suppressing the PI3K/AKT/NF-κB signaling pathway in vivo and in vitro.

Osteoarthritis (OA) is a serious and frequently occurring disease in the elderly, characterized by cartilage degeneration and proliferation of bone structure. Glycyrrhizin, a compound extracted from licorice, has been reported to have various important biological activities, such as antioxidant properties and anti-inflammatory action. However, it has not been reported whether glycyrrhizin has a positive effect on OA development. Our study aimed to evaluate the effects of glycyrrhizin on human OA chondrocytes. In the present study, we discovered that glycyrrhizin remarkably suppressed the interleukin (IL)-1β-induced level of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) and the production of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOs), metalloproteinase3 (MMP3), metalloproteinase13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin motifs5 (ADAMTS5). In addition, glycyrrhizin inverted the degradation of aggrecan and collagen II. Moreover, it significantly inhibited IL-1β-stimulated PI3K/AKT phosphorylation and NF-κB mobilization in human OA chondrocytes. In vivo, glycyrrhizin treatment prevented the destruction of cartilage in mice OA models. In summary, all the results demonstrate that glycyrrhizin may be a potential therapeutic approach for OA.
Ren-Hao Jiang, Jia-Jing Xu, Ding-Chao Zhu, Jia-Feng Li, Chen-Xi Zhang, Nan Lin, Wei-Yang Gao

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#31180546   2019/05/27 To Up

β‑catenin signalling inhibits cartilage endplate chondrocyte homeostasis in vitro.

Cartilaginous endplate degeneration serves a key role in the process of intervertebral disc (IVD) degeneration, however, effective therapies are hindered by an incomplete understanding of the mechanisms that underlie cartilage endplate (CEP) homeostasis and degeneration. Wnt/β‑catenin signalling has been reported as a major factor in regulating biological processes. Whether Wnt/β‑catenin signalling engages in CEP homeostasis has not yet been investigated. The present study aimed to assess the function of CEP cells via the activation of Wnt/β‑catenin signalling to examine and promote the mechanism of degeneration of CEP in vitro. Rat CEP cells were confirmed to exhibit a chondrocytic phenotype by toluidine blue staining. The increased number of senescence‑associated β‑galactosidase (SA‑β‑gal)‑positive cells and reduced cellular proliferation were investigated in the presence of a β‑catenin inhibitor, and the inhibitor improved the trend of senescence. An increased number of apoptotic cells was detected by lithium chloride treatment, and inhibiting Wnt/β‑catenin signalling protected the cells from apoptosis. Expression of the catabolic enzymes, metalloproteinase‑13 and a disintegrin and metalloproteinase with thrombospondin motifs‑5, and the decreased expression of aggrecan were also observed by Wnt/β‑catenin signalling activation, and a Wnt/β‑catenin signalling inhibitor decreased the expression of catabolic enzymes and increased the expression of aggrecan induced by Wnt/β‑catenin signalling activation. Wnt/β‑catenin signalling may provide potential strategies for preventing CEP degeneration.
Lei Ding, Zengxin Jiang, Jingping Wu, Defang Li, Houlei Wang, Wei Lu, Qingmin Zeng, Guoxiong Xu

1034 related Products with: β‑catenin signalling inhibits cartilage endplate chondrocyte homeostasis in vitro.

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#31123330   2019/05/23 To Up

Ras suppressor-1 (RSU-1) promotes cell invasion in aggressive glioma cells and inhibits it in non-aggressive cells through STAT6 phospho-regulation.

Most gliomas are invasive tumors formed from glial cells and associated with high mortality rates. In this study, we characterized four glioma cell lines of varying degree of aggressiveness (H4, SW1088, A172 and U87-MG) in terms of morphology, cytoskeleton organization and stiffness, and evaluated their invasive potential by performing invasion, colony forming and spheroid invasion assays. Cells were divided into two distinct groups: aggressive cell lines (A172 and U87-MG) with more elongated, softer and highly invasive cells and less aggressive cells (H4 and SW088). Interestingly, we found that Ras Suppressor-1 (RSU-1), a cell-matrix adhesion protein involved in cancer cell invasion, was significantly upregulated in more aggressive glioma cells compared to less aggressive. Importantly, RSU-1 silencing had opposing effects on glioma cell invasion depending on their aggressiveness, inhibiting migration and invasion of aggressive cells and promoting those of less aggressive cells. Finally, we found that RSU-1 silencing in aggressive cells led to decreased Signal Transducer and Activator of Transcription6 (STAT6) phosphorylation and Matrix Metalloproteinase13 (MMP13) expression in contrast to less invasive cells. Our study demonstrates that RSU-1 promotes invasion of aggressive glioma cells and inhibits it in the non-aggressive cells, indicating that it could serve as a predictor of gliomas progression.
Maria Louca, Andreas Stylianou, Angeliki Minia, Vaia Pliaka, Leonidas G Alexopoulos, Vasiliki Gkretsi, Triantafyllos Stylianopoulos

1224 related Products with: Ras suppressor-1 (RSU-1) promotes cell invasion in aggressive glioma cells and inhibits it in non-aggressive cells through STAT6 phospho-regulation.

1x10e7 cells96 wells1x10e7 cells1x10e7 cells1x10e7 cells1x10e7 cells100 µg96 tests-100 µg1 mg

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#30569095   2018/12/12 To Up

Theaflavins prevent cartilage degeneration via AKT/FOXO3 signaling in vitro.

Theaflavins (TFs) are the main bioactive polyphenols in tea and contribute to protection against oxidative stress. Excessive reactive oxygen species (ROS) accumulation can lead to the disruption of cartilage homeostasis. The present study examined the potential effects of TFs on H2O2‑induced cartilage degeneration in vitro. Cell Counting kit (CCK‑8) was used to determine cell viability, and flow cytometric analysis was used to detect ROS, apoptosis and DNA damage. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting were used to detect the expression levels of target factors. The present study revealed that TFs effectively reduced the expression of catabolic factors, including matrix metalloproteinase‑13, interleukin‑1 and cartilage glycoprotein 39. TFs inhibited ROS generation in cartilage degeneration, and suppressed apoptosis and DNA damage caused by oxidative stress. TFs also downregulated the expression levels of cleaved caspase‑3 and B‑cell lymphoma 2‑associated X protein, and the DNA damage‑related genes, ATR serine/threonine kinase and ATM serine/threonine kinase. Furthermore, TFs enhanced the activity of glutathione peroxidase 1 and catalase, but reduced the expression levels of phosphorylated (p)‑AKT serine/threonine kinase (AKT) and p‑Forkhead box O3 (FOXO3)a. Conversely, the effects of TFs on apoptosis and DNA damage were reversed by persistent activation of AKT. In conclusion, TFs prevented cartilage degeneration via AKT/FOXO3 signaling in vitro. The present study suggested that TFs may be a potential candidate drug for the prevention of cartilage degeneration.
Jun Li, Jianping Zheng

2564 related Products with: Theaflavins prevent cartilage degeneration via AKT/FOXO3 signaling in vitro.

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#29750304   2018/05/07 To Up

Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.

Vascular endothelial growth factor (VEGF) is expressed in articular cartilage and increases in expression levels have been associated with the progression of osteoarthritis (OA). Thalidomide is a drug that has been reported to inhibit angiogenesis and reduce VEGF production by downregulating VEGF expression. The objective of the present study was to determine whether intraperitoneal administration of thalidomide may attenuate early OA development in mice. Male C57BL/6 mice (10‑weeks‑old) were randomly assigned into the destabilization of the medial meniscus (Dmm) with thalidomide treatment (Dmm+Th), Dmm and Sham groups equally. An OA model was induced surgically in Dmm+Th and Dmm groups, and mice of the Dmm+Th group were subsequently treated with an intraperitoneal injection of thalidomide (200 mg/kg/day). At 2 and 4 weeks following surgery, the pathological alterations in cartilage samples were assessed qualitatively by hematoxylin and eosin staining and Safranin O/Fast green staining, and quantitatively by the Osteoarthritis Research Society International scoring system. The mRNA expression levels of matrix metalloproteinase‑13 (MMP‑13) and VEGF were measured by reverse transcription‑quantitative polymerase chain reaction. The protein expression levels of MMP‑13 and VEGF were detected by immunofluorescence and immunohistochemistry, respectively. The production of VEGF in serum was evaluated via an ELISA assay. Pathological scores were significantly higher in the Dmm and the Dmm+Th groups than those in the Sham group; however, the Dmm+Th group exhibited markedly less severe pathological changes compared with the Dmm group. Compared with the Sham group, the mRNA and protein expression levels of VEGF and MMP‑13 in the Dmm and the Dmm+Th groups were significantly increased. The Dmm+Th group exhibited significantly decreased expression levels of VEGF and MMP‑13, as well as significantly decreased serum VEGF concentration compared with the Dmm group. Thus, the results of the present study demonstrated that intraperitoneal administration of thalidomide may alleviate the development of early OA by suppressing VEGF expression in mice and may have potential as a novel therapy for the treatment of OA.
Jia Lin Song, De Long Li, Hang Fang, Dao Zhang Cai

2966 related Products with: Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.

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#29549926   2017/11/13 To Up

Expression of miR-206 in Human Knee Articular Chondrocytes and Effects of miR-206 on Proliferation and Apoptosis of Articular Chondrocytes.

Increasing evidence has demonstrated that microRNAs regulate the development of cartilage and osteogenesis. Whether miR-206 participates in the development of human articular cartilage remains largely unknown. This study aimed to investigate the role of miR-206 in human chondrocytes.
Zhe Ni, Xifu Shang, Guolin Tang, Lei Niu

1039 related Products with: Expression of miR-206 in Human Knee Articular Chondrocytes and Effects of miR-206 on Proliferation and Apoptosis of Articular Chondrocytes.

1000 5 G100ul100 4 Membranes/Box0.1 mg200 4 Arrays/Slide1 ml1 mg100.00 ug

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