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ursolic acid/hemorràgia

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Ursolic acid reduces oxidative stress to alleviate early brain injury following experimental subarachnoid hemorrhage.

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Ursolic acid (UA), a well-known anti-oxidative reagent, has been reported to protect the brain against ischemic stoke. However, the potential role of UA in protecting against early brain injury (EBI) after subarachnoid hemorrhage (SAH) remains unclear. The present study aimed to examine the effect
Neutrophil activation is associated with the development of organ injury after trauma-hemorrhagic shock. In the present study, ursolic acid inhibited the superoxide anion generation and elastase release in human neutrophils. Administration of ursolic acid attenuated trauma-hemorrhagic shock-induced

Ursolic acid alleviates early brain injury after experimental subarachnoid hemorrhage by suppressing TLR4-mediated inflammatory pathway.

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Our previous studies proved that ursolic acid (UA) protected against early brain injury (EBI) by modulating oxidative stress after experimental subarachnoid hemorrhage (SAH), but it has not been evaluated yet about its effects on an inflammatory pathway in a SAH model. This study was undertaken to

Betulinic, oleanolic and ursolic acids inhibit the enzymatic and biological effects induced by a P-I snake venom metalloproteinase.

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Betulinic acid (BA), Oleanolic acid (OA) and Ursolic acid (UA), are pentacyclic triterpenoids with widespread occurrence throughout the plant kingdom, these compounds are widely recognized by their pharmacological and biological properties, such as, anti-tumoral, anti-inflammatory, anti-microbial

Anti-angiogenic activity and antitumor efficacy of amphiphilic twin drug from ursolic acid and low molecular weight heparin.

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Heparin, a potential blood anti-coagulant, is also known for its binding ability to several angiogenic factors through electrostatic interactions due to its polyanionic character. However, the clinical application of heparin for cancer treatment is limited by several drawbacks, such as

[Triterpene saponins in Panax japonicus and their ~(13)C-NMR spectroscopic characteristics].

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Panax japonicus( PJ) is a valuable medicinal plant belonging to the genus Panax of Araliaceae,the recumbent rhizome of which is widely used in clinic therapy,healthcare products and as cosmetic additives with functions of dissipating stasis,reducing swelling,stanching bleeding,and reinforcing

Sigma receptor-mediated targeted delivery of anti-angiogenic multifunctional nanodrugs for combination tumor therapy.

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The potential of low molecular weight heparin (LMWH) in anti-angiogenic therapy has been tempered by poor in vivo delivery to the tumor cell and potentially harmful side effects, such as the risk of bleeding due to heparin's anticoagulant activity. In order to overcome these limitations and further

Antioxidant activity against H2O2-induced cytotoxicity of the ethanol extract and compounds from Pyrola decorate leaves.

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BACKGROUND The leaves of Pyrola decorate H. Andr (Pyrolaceae), known as Luxiancao, have long been used for treating kidney deficiency, gastric haemorrhage and rheumatic arthritic diseases in traditional Chinese medicine. OBJECTIVE The phytochemicals and antioxidant capacities in vitro of P. decorate

Triterpenoids from fruits of Sorbus pohuashanensis inhibit acetaminophen-induced acute liver injury in mice.

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Drug-related hepatotoxicity has become a serious social issue nowadays. Acetaminophen (APAP) was widely used in clinical treatment, although commonly acknowledged that it is a general material that caused drug-related hepatotoxicity. In this study, triterpenoids (Trds) which are mainly composed of

Triterpenes from Callicarpa integerrima Champ.

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A new triterpenoid saponin and fourteen known triterpenoids were isolated from the methanol extract of the stems and leaves of Callicarpa integerrima Champ, which is used in Chinese folk medicine for stopping bleeding, expelling the wind, dissipating stagnation, and treating scrofula, by using

Fruit-Derived Polysaccharides and Terpenoids: Recent Update on the Gastroprotective Effects and Mechanisms.

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Ulceration in the stomach develops in peptic ulcer disease when there is a loss of protective mucosal layers, particularly in Helicobacter pylori infection. Antibiotic therapy has failed to eradicate and impede the colonization of H. pylori. Despite given treatment, recurrent bleeding can occur and
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