madecassoside/kanker

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Protective effects of madecassoside against Doxorubicin induced nephrotoxicity in vivo and in vitro.

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Madecassoside (MA), a triterpenoid saponin isolated from C. asitica, exerts various pharmacological activity including antioxidative and antinflammatory. Doxorubicin (DOX), a common chemotherapeutic drug, has been reported to induce numerous toxic side effects including renal-toxicity. We

Madecassoside attenuates inflammatory response on collagen-induced arthritis in DBA/1 mice.

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Madecassoside (MA), a triterpenoid product isolated from Centella asiatica, has been described to exhibit antioxidant and anti-inflammatory activities. The present study was undertaken to determine whether madecassoside (MA) is efficacious against collagen-induced arthritis (CIA) in mice and its

Madecassoside prevents Aβ(25-35)-induced inflammatory responses and autophagy in neuronal cells through the class III PI3K/Beclin-1/Bcl-2 pathway.

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Inflammatory responses and autophagy have been implicated in the amyloid-β (Aβ) aggregation in Alzheimer's disease (AD) due to recycling cellular waste and eliminating toxic protein aggregates. Madecassoside (Mad), a triterpenoid saponin compound, has been found to improve impaired cognitive

Neuroprotective effects of madecassoside against focal cerebral ischemia reperfusion injury in rats.

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Madecassoside, a triterpenoid derivative isolated from Centella asiatica, exhibits anti-inflammatory and antioxidant activities. We investigated its neuroprotective effect against ischemia-reperfusion (I/R) injury in cerebral neurons in male Sprague-Dawley rats. Madecassoside (6, 12, or 24mg/kg,

Madecassoside protects BV2 microglial cells from oxygen-glucose deprivation/reperfusion-induced injury via inhibition of the toll-like receptor 4 signaling pathway.

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In a previous study, the authors reported that madecassoside (MA) exerted a potent neuroprotective effect against cerebral ischemia-reperfusion (I/R) injury in rats, mediated by anti-oxidative, anti-inflammatory, and anti-apoptotic mechanisms. However, the cellular and molecular bases for its

Madecassoside ameliorates lipopolysaccharide-induced neurotoxicity in rats by activating the Nrf2-HO-1 pathway.

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Neuroinflammation is a predisposing factor for several neurodegenerative diseases. The purpose of this study was to evaluate the protective effect of madecassoside (MA) in lipopolysaccharide (LPS)-induced cognitive impairment and neuroinflammation in rats. MA has many protective effects such as

Madecassoside prevents acute liver failure in LPS/D-GalN-induced mice by inhibiting p38/NF-κB and activating Nrf2/HO-1 signaling.

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Madecassoside (MA), a triterpenoid saponin isolated from Centella asiatica, exerts various pharmacological activities including antioxidative and anti-inflammatory effects. The aim of this study was to explore the protective effect of MA in the treatment of lipopolysaccharide (LPS) and

Madecassoside suppresses proliferation and invasiveness of HGF-induced human hepatocellular carcinoma cells via PKC-cMET-ERK1/2-COX-2-PGE2 pathway.

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Recent studies showed that Madecassoside (MAD), a pentacyclic triterpene isolated from Centella asitica (L.), was used as a therapeutic agent in wound healing and also as an anti-inflammatory, anti-oxidative activities and anti-aging agent. However, its role in cancer has not been elucidated. In our

Protection of mouse brain from paracetamol-induced stress by Centella asiatica methanol extract.

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Centella asiatica (CA) is a medicinal herb traditionally used as a brain tonic in Ayurvedic medicine. Various ethnomedical leads revealed the effective use of CA in the treatment of symptoms associated to oxidative stress and inflammation.The aim of this

Anti-inflammatory effects of madecassic acid via the suppression of NF-kappaB pathway in LPS-induced RAW 264.7 macrophage cells.

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We have investigated the anti-inflammatory effects of madecassic acid and madecassoside isolated from Centella asiatica (Umbelliferae) on lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophage cells. Both madecassic acid and madecassoside inhibited the production of nitric oxide (NO),

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