Momilactone B, an allelochemical of rice hulls, induces apoptosis on human lymphoma cells (Jurkat) in a micromolar concentration.

Although momilactone B has been studied as an allelochemical of rice (Oryza sativa L.), to date we have no report showing the effect of momilactone B on mammalian cells. This study was undertaken to examine whether this allelochemical has anticancer activity on cancer cells. We show here that momilactone B at micromolar doses has antitumor efficacy by inducing apoptosis in several blood cancer cells including human leukemic T cells. In addition, our study elucidated that anticancer activity of momilactone B on human leukemic T cells resulted from the induction of apoptosis via caspase and mitochondria. From these results, momilactone B can be considered as a novel therapeutic strategy for human leukemic T cells from its direct apoptosis-inducing activity.

Clematis mandshurica protected to apoptosis of rat chondrocytes.

OBJECTIVE: To investigate the effect of SKI 306X, a purified extract from the mixture of three herbs, i.e. Clematis mandshurica, Trichosanthes kirilowii and Prunella vulgaris, on apoptosis in chondrocytes. DESIGN: Rat chondrocyte cell line RCJ3.1C.18 cells were incubated with 1 microM staurosporin and SKI 306X or each of its components. Cell viability was determined by trypan blue exclusion assay. Induction of apoptosis was determined by nuclear condensation or fragmentation after Hoechst staining. Amount of apoptosis was quantified both by nuclear morphology and flow cytometry. Expression level of Bcl-2, and caspase-3 and PARP activations were assayed by Western blot. RESULTS: SKI 306X significantly prevented staurosporin-induced apoptosis. Among its three components, only Clematis mandshurica significantly decreased the amount of staurosporin-induced apoptosis. Although the level of Bcl-2 expression was decreased after staurosporin treatment, it was sustained after the combination treatment with Clematis mandshurica. Whereas staurosporin induced the degradation of 32 kDa caspase-3 precursor and the production of 85-kDa cleavage products of PARP in a time-dependent fashion, Clematis mandshurica treatment prevented those manifestations. CONCLUSIONS: Pharmacological efficacy of SKI 306X protecting osteoarthritis in part may result from the inhibition of apoptosis in chondrocytes by Clematis mandshurica.

Magnoliae flos induces apoptosis of RBL-2H3 cells via mitochondria and caspase.

BACKGROUND: Magnoliae flores (MF), the buds of Magnolia denudata Desrousseaux, have been successfully used for the management of allergic diseases in Korea. The purpose of the present study was to determine their causal role in inducing apoptosis of mast cells and to verify the underlying mechanism. METHODS: The viability of mast cells was assessed by the trypan blue exclusion test. Induction of apoptosis was confirmed by DNA fragmentation, nuclear staining and DNA hypoploidy. Western blotting and immunofluorescent staining were performed to study the alterations in expression level and translocation of apoptosis-related proteins. Mitochondrial membrane potential (MMP) change and cytochrome C release were assayed. RESULTS: We present several lines of evidence indicating that MF induce apoptosis. Changes in cell morphology, generation of DNA fragmentation, cell cycle arrest, activation of caspase-3, and PARP and DFF degradations were demonstrated. The reduction of MMP and the release of cytochrome C to cytosol were also shown. Either PTP blockers, bongkrekic acid and cyclosporin A, or pancaspase inhibitors, Boc.D-fmk and zVAD-fmk, did not prevent the release of cytochrome C. Bax protein content was increased, and Bax was translocated from cytosol into mitochondria at early time points after MF treatment. CONCLUSIONS: We have demonstrated that MF induce mitochondria- and caspase-dependent mast cell apoptosis. Our observations contribute new insights to the role of MF and support the view that the clinical effect of MF may depend on their pharmacological efficacy in regulating mast cell apoptosis.

Genistein-induced apoptosis of p815 mastocytoma cells is mediated by Bax and augmented by a proteasome inhibitor, lactacystin.

Although genistein has been demonstrated to induce apoptosis of various cells, there is no report of its effect on mast cell proliferation. Here we show that genistein reduced the viability of mast cell tumor cell lines, p815 and RBL-2H, but not of a human mast cell line, HMC-1. Further investigation on its growth-inhibitory mechanism was undertaken on p815 mastocytoma cells. Genistein induced G2/M arrest and subsequent apoptotic death. p815 cells undergoing apoptosis showed many apoptotic manifestations, such as reduction of mitochondrial membrane potential, release of cytochrome c to cytosol, translocation of apoptosis-inducing factor to nucleus, activation of caspase-3, nuclear condensation, and generation of DNA fragmentation. Genistein treatment resulted in the increase of Bax expression and its translocation into mitochondria, whereas expression levels of Bcl-2 remained unchanged. Proteasome activity decreased at the early time points after genistein treatment, but thereafter it fluctuated at increased levels. A proteasome inhibitor, lactacystin, potentiated the induction of apoptosis. Taken together, genistein-induced apoptosis of p815 mastocytoma cells is at least in part mediated by proteasome, Bax, apoptosis-inducing factor, and caspase and augmented by cotreatment with a proteasome inhibitor, lactacystin.