Protective effects of green tea polyphenol against cisplatin-induced nephrotoxicity in rats.

Objective: This study is to compare the effects of green tea polyphenol (GTP) pre-treatment with those of GTP post-treatment on cisplatin (CP)-induced nephrotoxicity in rat.

Methods: Male Sprague-Dawley rats were randomly divided into six groups. Animals in the control group received 0.

Photodynamic therapy for breast cancer in a BALB/c mouse model.

Objective: Photodynamic therapy (PDT) has been used for superficial neoplasms and its usage has been recently extended to deeper lesions. The purpose of this study was to observe whether or not PDT can cure breast cancer in the solid tumor model, and to define the critical point of laser amount for killing the cancer cells.

Methods: Twenty four BALB/c mouse models with subcutaneous EMT6 mammary carcinomas were prepared.

Successful full term pregnancy and delivery after concurrent chemo-photodynamic therapy (CCPDT) for the uterine cervical cancer staged 1B1 and 1B2: Preserving fertility in young women.

► Photodynamic therapy can treat lesions with highly reactive single oxygen. ► CCPDT (Concurrent Chemo Photodynamic Therapy) is defined as PDT with chemotherapy. ► CCPDT can treat larger and deeper lesions than PDT due to PCI concept.

Renoprotective effects of green tea extract on renin-angiotensin-aldosterone system in chronic cyclosporine-treated rats.

Background: Renin-angiotensin-aldosterone system (RAAS) activation plays an important role in cyclosporine (CsA)-induced nephropathy. The main aim of this study was to test whether the administration of green tea extract (GTE) prevents the development of CsA-induced nephrotoxicity.

Methods: The rats were treated for 21 days and divided into four groups (n = 6/group): control group (0.

The protective effects of green tea extract against L-arginine toxicity to cultured human mesangial cells.

The aim of this study was to investigate whether green tea extract (GTE) has the protective effects on excess L-arginine induced toxicity in human mesangial cell. Human mesangial cells treated with L-arginine were cultured on Dulbecco's modified eagle medium in the presence and absence of inducible nitric oxide synthase (iNOS) inhibitor and GTE. The cell proliferation was determined by 3 (4,5-dimethylthiazol-2-yl)-2, 5-diphengltetrqzolium bromide, a tetrazole assay.

hMTH1 depletion promotes oxidative-stress-induced apoptosis through a Noxa- and caspase-3/7-mediated signaling pathway.

Although the accumulation of 8-oxo-dGTP in DNA is associated with apoptotic cell death and mutagenesis, little is known about the exact mechanism of hMTH1-mediated suppression of oxidative-stress-induced cell death. Therefore, we investigated the regulation of DNA-damage-related apoptosis induced by oxidative stress using control and hMTH1 knockdown cells. Small interfering RNA (siRNA) was used to suppress hMTH1 expression in p53-proficient GM00637 and H460 cells, resulting in a significant increase in apoptotic cell death after H(2)O(2) exposure; however, p53-null, hMTH1-deficient H1299 cells did not exhibit H(2)O(2)-induced apoptosis.

Activity of green tea polyphenol epigallocatechin-3-gallate against ovarian carcinoma cell lines.

Purpose: A constituent of green tea, (-)-epigallocatechin-3-gallate (EGCG), is known to possess anti-cancer properties. In this study, the time-course of the anticancer effects of EGCG on human ovarian cancer cells were investigated to provide insights into the molecular-level understanding of the growth suppression mechanism involved in EGCG-mediated apoptosis and cell cycle arrest.

Materials And Methods: Three human ovarian cancer cell lines (p53 negative, SKOV-3 cells; mutant type p53, OVCAR-3 cells; and wild type p53, PA-1 cells) were used.

The molecular mechanism of Noxa-induced mitochondrial dysfunction in p53-mediated cell death.

Genotoxic stresses stabilize the p53 tumor suppressor protein which, in turn, transactivates target genes to cause apoptosis. Although Noxa, a "BH3-only" member of the Bcl-2 family, was shown to be a target of p53-mediated transactivation and to function as a mediator of p53-dependent apoptosis through mitochondrial dysfunction, the molecular mechanism by which Noxa causes mitochondrial dysfunction is largely unknown. Here we show that two domains (BH3 domain and mitochondrial targeting domain) in Noxa are essential for the release of cytochrome c from mitochondria.