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Last update 08 May 2025

MMPs x NOS2

Last update 08 May 2025

Basic Info

Related Targets

MMPsNOS2

Drugs associated with MMPs x NOS2

CR-3294

Target

MMPs x NOS2

Mechanism

MMPs inhibitors [+1]

Active Org.-

Originator Org.

Rottapharm SpA

Active Indication-

Inactive Indication

Diarrhea [+2]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with MMPs x NOS2

EUCTR2010-020660-37-IT

/ Not yet recruitingNot Applicable

A Multicenter, randomized, double blind, double dummy, placebo controlled, parallel group, phase II study on the prevention of mucositis by CR3294, orally administered for 5 days in haematological patients receiving high dose chemotherapy followed by autologous stem cell transplantation. - ND

Start Date08 Sep 2010

Sponsor / Collaborator-

100 Clinical Results associated with MMPs x NOS2

100 Translational Medicine associated with MMPs x NOS2

0 Patents (Medical) associated with MMPs x NOS2

1,554

Literatures (Medical) associated with MMPs x NOS2

01 Dec 2025·Molecular Biology Reports

Edaravone reduces brain injury in hepatic encephalopathy by upregulation of Nrf2/HO-1 and inhibition of NF-κB, iNOS/NO and inflammatory cytokines

Article

Author: Imani, Mahsa ; Amirshahrokhi, Keyvan

BACKGROUNDBrain damage is the most important complication in patients with hepatic encephalopathy (HE). Oxidative stress and inflammation are essential factors in the progression of brain injury caused by HE. The aim of this study was to investigate the potential therapeutic effect of edaravone and its underlying mechanisms against brain injury associated with HE in mice.METHODS AND RESULTSHE was induced by the injection of thioacetamide (200 mg/kg) for 2 days and then mice treated with edaravone (10 or 20 mg/kg/day, ip) for four consecutive days. The brain tissues were dissected for histopathological, biochemical, ELISA, RT-qPCR and immunofluorescence analysis. The results showed that edaravone improved the locomotor function and ameliorated brain histopathological changes in mice with HE. Edaravone inhibited oxidative stress markers by increasing the levels of glutathione, catalase, superoxide dismutase, glutathione reductase and the upregulation of nuclear erythroid 2-related factor (Nrf2)/HO-1 pathway in the brain tissue. Administration of edaravone significantly decreased the expression of p-NF-κB and iNOS. Edaravone treatment reduced the levels of NO, MPO and MMP-9 in the brain of mice. Additionally, the brain levels and expressions of inflammatory cytokines IL-1β, IL-6, TNF-α and IFN-γ were downregulated in mice treated with edaravone.CONCLUSIONSThese results suggest that edaravone exerts significant neuroprotection by modulating of inflammatory and oxidative responses in HE and may serve as a promising agent for the treatment of brain injury associated with HE.

01 Jun 2025·Tissue and Cell

Terminalia chebula fruit extract attenuates LPS-induced acute lung injury in mouse model

Article

Author: Singh, Vidya ; Aneesha, V A ; Sharma, Meemansha ; Singh, Thakur Uttam ; Sharma, Anshuk ; Lingaraju, Madhu Cholenahalli ; Gari, Manju ; Shanker, Karuna

This study evaluated the pretreatment effect of ethanolic extract of Terminalia chebula fruit (TCE) on LPS-induced acute lung injury in mice. TCE doses of 100 and 200 mg/kg bwt were administered for seven days before LPS exposure. Pretreatment effects were assessed by measuring lung oedema, total protein, MPO, ferritin, D-dimer, oxidative stress, and histopathology, along with iNOS, and MMP-9 expression. TCE pretreatment reduced lung edema, total protein, MPO, ferritin, and D-dimer levels significantly. It also decreased MDA content while enhancing antioxidant enzymes catalase and glutathione. Histopathology showed moderate lung injury reduction at 200 mg/kg bwt TCE, with less neutrophilic infiltration and better lung tissue architecture. Furthermore, the administration of TCE significantly reduced the expression of iNOS and MMP-9. Thus, TCE pretreatment alleviates LPS-induced acute lung injury by reducing inflammatory markers and oxidative stress.

01 Jun 2025·Experimental Gerontology

Baicalin alleviates intervertebral disc degeneration by inhibiting the p38 MAPK signaling pathway

Article

Author: Zhu, Zezhang ; Qiu, Yong ; Li, Fengrui ; Wu, Yating ; Shu, Shibin ; Li, Sen ; Feng, Zhenhua

BACKGROUNDIntervertebral disc degeneration (IVDD) represents a prevalent degenerative pathology of the spinal, primarily precipitated by inflammatory processes and the deterioration of extracellular matrix (ECM). Baicalin has an effective anti-inflammatory effect on degenerative diseases. In addition, the P38 mitogen-activated protein kinase (MAPK) signaling pathway plays a crucial role in the pathogenesis of IVDD.OBJECTIVETo investigate the therapeutic potential of baicalin in modulating pathological changes in IVDD.METHODSTo design an in vitro model of degeneration of nucleus pulposus cells (NPCs) stimulated by IL-1β and an in vivo mouse model of needling to assess the protective effect of baicalin against IVDD and its underlying mechanism.RESULTSBaicalin down-regulated inflammatory factors (INOS, COX-2, IL-6) and catabolic factors (MMP-3, MMP-13, ADAMTS-5) while up-regulating anabolic factors (collagen II, SOX-9) by inhibiting the activation of the p38 MAPK signaling pathway, in addition to slowing down the progression of IVDD in the mouse acupuncture model.CONCLUSIONOur study demonstrated in vitro experiments that baicalin attenuates IL-1β-stimulated IVDD by inhibiting activation of the P38 MAPK signaling pathway. Meanwhile, the effects of baicalin were also confirmed in vivo experiments, Consequently, we propose that baicalin is a promising therapeutic agent for the treatment of disc degeneration.

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