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oxymatrine/nekrosis
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Oxymatrine exhibits anti-neuroinflammatory effects on Aβ1-42-induced primary microglia cells by inhibiting NF-κB and MAPK signaling pathways.
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Oxymatrine (OMT), isolated from Sophora flavescens or Sophora alopecuroides, possesses various pharmacological and biological activities, including anti-inflammatory, anti-oxidant, and anti-diabetic properties. Microglia cells, the resident immune cells in the central nervous system (CNS), play a
Anti-inflammatory mechanism of oxymatrine in dextran sulfate sodium-induced colitis of rats.
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OBJECTIVE
To investigate the anti-inflammatory mechanism of oxymatrine in dextran sulfate sodium (DSS)-induced colitis of rats.
METHODS
Acute colitis was induced by giving 2% DSS orally in drinking water for 8 d. Twenty-six male rats were randomized into oxymatrine-treated group (group A, 10 rats),
Oxymatrine alleviates periodontitis in rats by inhibiting inflammatory factor secretion and regulating MMPs/TIMP protein expression1.
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To investigate the effect of oxymatrine on periodontitis in rats and related mechanism. Methods: Ninety SD rats were divided into control, model, 10, 20 and 40 mg/kg oxymatrine and tinidazole groups. The periodontitis model was established in later 5 groups. The 10, 20 and 40 mg/kg oxymatrine groups
Oxymatrine inhibits lipopolysaccharide-induced inflammation by down-regulating Toll-like receptor 4/nuclear factor-kappa B in macrophages.
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Oxymatrine (OMT) is the quinolizidine alkaloid extracted from the Chinese herb Sophora flavescens Ait. that has many pharmacological effects and is used for the treatment of some inflammatory diseases. In this study, RAW264.7 cells and THP-1 differentiated macrophages were pretreated with various
Oxymatrine provides protection against Coxsackievirus B3-induced myocarditis in BALB/c mice.
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Oxymatrine is the primary pharmacological component of Sophora flavescens Ait. In the present study, we investigated the protective effect of oxymatrine against Coxsackievirus B3-induced myocarditis in mice. Coxsackievirus B3-infected HeLa cells were treated with oxymatrine and the viral titer, as
Oxymatrine attenuates intestinal ischemia/reperfusion injury in rats.
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OBJECTIVE
Intestinal ischemia/reperfusion (I/R) is a common and serious clinical condition. The anti-inflammatory and anti-apoptotic properties of oxymatrine, the extract from a traditional Chinese herb, Sophora flavescens Ait, have been shown to protect the liver from I/R injury and attenuate
Anti‑inflammatory effects of oxymatrine on rheumatoid arthritis in rats via regulating the imbalance between Treg and Th17 cells.
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Oxymatrine (OMT), a monosomic alkaloid extracted from the Chinese herb, Sophora flavescens Ait, has long been used as a traditional Chinese medicine for the treatment of inflammatory diseases. The aim of the present study was to investigate the potential anti‑inflammatory effect of OMT, and its
Oxymatrine attenuates bleomycin-induced pulmonary fibrosis in mice via the inhibition of inducible nitric oxide synthase expression and the TGF-β/Smad signaling pathway.
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Oxymatrine (OM) is an alkaloid extracted from the Chinese herb Sophora flavescens Ait. with a variety of pharmacological activities. The aim of this study was to investigate the preventive effects of OM on bleomycin (BLM)-induced pulmonary fibrosis (PF) and to further explore the underlying
Oxymatrine reduces neuroinflammation in rat brain: A signaling pathway.
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Cerebral neuroinflammation models were established by injecting 10 μg lipopolysaccharide into the hippocampus of male Sprague-Dawley rats. The rats were treated with an intraperitoneal injection of 120, 90, or 60 mg/kg oxymatrine daily for three days prior to the lipopolysaccharide injection.
[Effect of oxymatrine on pathological change in brain tissue of newborn mice infected by cytomegalovirus].
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OBJECTIVE
To study the effect of oxymatrine on pathological change in brain tissue of newborn mice infected by cytomegalovirus (CMV).
METHODS
CMV of TCID50 was inoculated into the brain of the newborn mice, and the morphological change in the brain tissue infected by CMV was observed with light
Protective effect of oxymatrine against renal ischemia/reperfusion injury in rats.
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Renal ischemia/reperfusion (I/R) injury is a common cause of acute kidney injury. The pathologic mechanisms underlying renal I/R injury are complicated, involving reactive oxygen species, necrosis, cell apoptosis, and inflammation, but the exact mechanisms remain unclear.
This study aimed to
[Effect of oxymatrine on JAK/STAT iteral in rat lung tissue with sepsis].
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OBJECTIVE
To explore the effects of oxymatrine (OMT) on JAK/STAT iteral in rat lung tissue with sepsis.
METHODS
Fifty-six male SD rats were randomly divided into 6 groups: sham operation group, model (CLP) group, CLP + OMT high, middle, low-dose groups (52, 26, 13 mg x kg(-1), vena caudalis bolus),
Oxymatrine inhibits renal fibrosis of obstructive nephropathy by downregulating the TGF-β1-Smad3 pathway.
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This study investigated whether oxymatrine (OMT) treatment can ameliorate renal interstitial fibrosis in unilateral ureteral obstruction (UUO) mice model. Moreover, the potential mechanisms of such treatment were analyzed. Twenty-four C57/BL6 mice were randomly divided into three groups, namely sham
[Effect of oxymatrine on NF-kappaB and other cell factors in rats lung tissue with septic shock].
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OBJECTIVE
To explore the effects of oxymatrine (OMT) on NF-kappaB and other cell factors in rat lung tissue with septic shock.
METHODS
Fifty-six male SD rats were randomly divided into 7 groups: sham operation group, OMT control group, model (CLP) group, CLP + OMT high, middle, low-dose group,
Oxymatrine reduces neuronal cell apoptosis by inhibiting Toll-like receptor 4/nuclear factor kappa-B-dependent inflammatory responses in traumatic rat brain injury.
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OBJECTIVE
To investigate the influence of oxymatrine (OMT) on Toll-like receptor 4 (TLR-4)/nuclear factor kappa-B (NF-κB)-dependent inflammatory responses and neuronal cell apoptosis after traumatic brain injury (TBI).
METHODS
Wistar rats were given an intraperitoneal injection of 60 or 120 mg/kg
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