picroside ii/воспаление

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Picroside II Protects Rat Lung and A549 Cell Against LPS-Induced Inflammation by the NF-κB Pathway.

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Picroside II is the main active ingredient in the root department of Chinese medicine Picrorhiza scrophulariiflora which has been proved to have beneficial effects on health, such as ameliorating the cerebral ischemia and protecting the liver. However, its effects on acute lung injury remain

Picroside II protects against sepsis via suppressing inflammation in mice.

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Picroside II, an iridoid compound extracted from Picrorhiza, exhibits anti-inflammatory and anti-apoptotic activities. We explored the protective effects and mechanisms of picroside II in a mouse model of sepsis induced by cecal ligation and puncture (CLP), using three groups of mice: Group A

Anti-inflammation effects of picroside 2 in cerebral ischemic injury rats.

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BACKGROUND Excitatory amino acid toxicity, oxidative stress, intracellular calcium overload, as well as inflammation and apoptosis are involved in the pathological process after cerebral ischemic reperfusion injury. Picrodide 2 could inhibit neuronal apoptosis and play anti-oxidant and

Picroside II Improves Severe Acute Pancreatitis-Induced Intestinal Barrier Injury by Inactivating Oxidative and Inflammatory TLR4-Dependent PI3K/AKT/NF-κB Signaling and Improving Gut Microbiota.

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Background

Picroside II exerts anti-inflammatory and antidiarrheal effects for treating the diseases associated with oxidative injury. However, its function on pancreatitis-induced intestinal barrier injury remains unclear. Hypothesis/Purpose. We hypothesized that

Picroside II protects rat kidney against ischemia/reperfusion-induced oxidative stress and inflammation by the TLR4/NF-κB pathway.

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Picroside II possesses a wide range of pharmacological effects and has been demonstrated to ameliorate cerebral ischemia and reperfusion (I/R) injury. However, its effects on renal I/R injury remain unclear. In the present study, the role of picroside II in attenuating oxidative stress and the

Picroside II attenuates hyperhomocysteinemia-induced endothelial injury by reducing inflammation, oxidative stress and cell apoptosis.

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Picroside II (P-II), one of the main active components of scrophularia extract, which have anti-oxidative, anti-inflammatory effects, but its effect on hyperhomocysteinemia (HHcy) induced endothelial injury remains to be determined. Here, we test whether P-II protects HHcy-induced endothelial

Neutrophilic Lung Inflammation Suppressed by Picroside II Is Associated with TGF-β Signaling.

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Although acute lung injury (ALI) is a leading cause of death in intensive care unit, effective pharmacologic means to treat ALI patients are lacking. The rhizome of Picrorhiza scrophulariiflora used in a traditional herbal medicine in Asian countries has been shown to have anti-inflammatory

Picroside II protects myocardium from ischemia/reperfusion-induced injury through inhibition of the inflammatory response.

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The inflammatory response is important in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Picroside II, the primary active constituent of Picrorhizae, has been reported to protect the myocardium from I/R-induced injury, however, the exact mechanism underlying these protective

The beneficial pharmacological effects and potential mechanisms of picroside II: Evidence of its benefits from in vitro and in vivo

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Picrorhiza kurroa, the dried rhizome of Picrorhiza kurroa Royle ex Benth, is a famous Chinese herb that has been traditionally used in China. Picroside II (PII), a glycoside derivative, is the main bioactive constituent of Picrorhiza kurroa. In the past several decades, bioactive components from

Picroside II decreases the development of fibrosis induced by ischemia/reperfusion injury in rats.

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In kidney transplantation, renal ischemia and reperfusion injury was one of the leading factors to the development of renal fibrosis, which was the main cause of graft loss. The fibrogenic changes were associated with the long term inflammation elicited by ischemia and reperfusion injury. In the

[Effect of Picroside II on ERK1/2 Signal Pathway in Cerebral lschemic Injury Rats].

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OBJECTIVE To explore the neuroprotective effect and mechanism of picroside II on extracellular regulated protein kinases1/2 (ERK1/2) signal transduction pathway in cerebral ischemia injuryrats. METHODS The middle cerebral artery occlusion (MCAO) model was established by inserting a monofilament into

Neuroprotective effect of picroside II in brain injury in mice.

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Various types of brain injury which led to the damage of brain tissue structure and neurological dysfunction continues to be the major causes of disability and mortality. Picroside II (PII) possesses a wide range of pharmacological effects and has been proved to ameliorate ischemia and reperfusion

[Effect of picroside II on expressions of TLR4 and NFkappaB in rats with cerebral ischemia reperfusion injury].

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OBJECTIVE To explore the effects of picrodide II on the expressions of Toll-like receptor 4 (TLR4) and nuclear transcription factor kappaB (NFkappaB) in brain tissue of rat after cerebral ischemic reperfusion (I/R) injury. METHODS Ten rats from 60 adult healthy female Wistar rats received

Picroside II Inhibits the MEK-ERK1/2-COX2 Signal Pathway to Prevent Cerebral Ischemic Injury in Rats.

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The objective of this study is to explore the neuroprotective effect and mechanism of picroside II on ERK1/2-COX2 signal transduction pathway after cerebral ischemic injury in rats. Focal cerebral ischemic models were established by inserting monofilament threads into the middle cerebral artery in

Picroside II Isolated from Pseudolysimachion rotundum var. subintegrum Inhibits Glucocorticoid Refractory Serum Amyloid A (SAA) Expression and SAA-induced IL-33 Secretion.

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Chronic obstructive pulmonary disease (COPD) is a major inflammatory lung disease characterized by irreversible and progressive airflow obstruction. Although corticosteroids are often used to reduce inflammation, steroid therapies are insufficient in patients with refractory COPD. Both serum amyloid

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