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decalepis arayalpathra/hemoterapija
Veza se sprema u međuspremnik
5 rezultati
Cyclophosphamide, a cancer chemotherapy drug-induced early onset of reproductive senescence and alterations in reproductive performance and their prevention in mice
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Although, cyclophosphamide (CP) treatment is known to cause degeneration of the ovarian follicular reserve, which may have a serious consequence of the onset of early reproductive senescence, thus far there is no experimental study either to demonstrate CP-induced early onset of reproductive
Antimetastatic pectic polysaccharide from Decalepis hamiltonii; galectin-3 inhibition and immune-modulation.
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Melanoma is a malignant neoplasm of major concern because of its high mortality rate and failure of chemotherapy. Previously we have shown that galectin-3, a galactose specific lectin, plays a pivotal role in the initiation of metastasis. It was hypothesized that blocking galectin-3 with galactose
Neuroprotective effect of Decalepis hamiltonii on cyclophosphamide-induced oxidative stress in the mouse brain.
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BACKGROUND
Cyclophosphamide (CP), one of the most widely used antineoplastic drugs, causes toxic side effects on vital organs including brain. In this study, we have investigated neuroprotective potential of the aqueous extract of the roots of Decalepis hamiltonii (DHA) against CP-induced oxidative
Chemoprotective effect of Decalepis hamiltonii against cyclophosphamide induced toxicity.
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Cancer is a hyper-proliferative disorder that involves transformation, dysregulation of apoptosis, Proliferation, invasion, angiogenesis and metastasis. The conventional methods to treat cancer are surgery, radiotherapy and chemotherapy. Chemotherapy, being a major treatment modality used for the
Amelioration of cyclophosphamide-induced hepatotoxicity by the root extract of Decalepis hamiltonii in mice.
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Hepatoprotective potential of the aqueous extract of the roots of Decalepis hamiltonii (DHA) against cyclophosphamide (CP)-induced oxidative stress has been investigated in mice. Administration of CP (25mg/kg b.w., i.p) for 10 days induced hepatic damage as indicated by the serum marker enzymes
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