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Gamma-tocotrienol, a major component of tocotrienol-rich fraction of palm oil, has been suggested to exhibit bone protective effects in vivo. However, the effects of -tocotrienol on osteoblast cells are still unclear. In this study, the effects of -tocotrienol on the proliferation, differentiation, and mineralization in osteoblastic MC3T3-E1 cells were investigated. Our results showed that -tocotrienol (2-8 mol/L) significantly improved the cell proliferation ( < 0.05), but it did not affect cell cycle progression.-Tocotrienol significantly increased alkaline phosphatase (ALP) activity ( < 0.05), secretion levels of osteocalcin (OC) and osteonectin (ON), and mRNA levels of collagen type I (Col I) of MC3T3-E1 cells. Meanwhile, we found that -tocotrienol is promoted in differentiation MC3T3-E1 cells by upregulation of the expression of Runx2 protein. Moreover, the number of bone nodules increased over 2.5-fold in cells treated with -tocotrienol (2-8 mol/L) for 24 d compared to control group. These results indicated that -tocotrienol at low dose levels, especially 4 mol/L, could markedly enhance the osteoblastic function by increasing the proliferation, differentiation, and mineralization of osteoblastic MC3T3-E1 cells. Moreover, our data also indicated that Runx2 protein may be involved in these effects. Further studies are needed to determine the potential of -tocotrienol as an antiosteoporotic agent.

γ-Tocotrienol, a kind of isoprenoid phytochemical, has antitumor activity. However, there is limited evidence that it has an effect on cervical cancer. In this study, the capacity to inhibit proliferation and induce apoptosis in human cervical cancer HeLa cells and the mechanism underlying these effects were examined. The results indicated that a γ-tocotrienol concentration over 30 μM inhibited the growth of HeLa cells with a 50% inhibitory concentration (IC50) of 46.90 ± 3.50 μM at 24 h, and significantly down-regulated the expression of proliferative cell nuclear antigen (PCNA) and Ki-67. DNA flow cytometric analysis indicated that γ-tocotrienol arrested the cell cycle at G0/G1 phase and reduced the S phase in HeLa cells. γ-tocotrienol induced apoptosis of HeLa cells in a time- and dose-dependent manner. γ-tocotrienol-induced apoptosis in HeLa cells was accompanied by down-regulation of Bcl-2, up-regulation of Bax, release of cytochrome from mitochondria, activation of caspase-9 and caspase-3, and subsequent poly (ADP-ribose) polymerase (PARP) cleavage. These results suggested that γ-tocotrienol could significantly inhibit cell proliferation through G0/G1 cell cycle arrest, and induce apoptosis via the mitochondrial apoptotic pathway in human cervical cancer HeLa cells. Thus, our findings revealed that γ-tocotrienol may be considered as a potential agent for cervical cancer therapy.

Bacillus velezensis W1, isolated from two-spotted spider mites that had died naturally, is a patented strain with strong capability to cause mortality of the phytophagous mite Tetranychus urticae. The whole genome of W1 was completely sequenced with a combination of an Illumina Miseq platform (400-bp paired-end) with 2 × 250 bases and a Pacific Biosciences (PaBio) RS II Single Molecule Real Time (SMRT) sequencing platform using a 20 kb SMRTbell TM template library. Here, we report the complete genome sequence of B. velezensis W1, including one circular chromosome of 4,237,431 bp encoding 4,352 genes with GC content of 45.84%, providing insights into the genomic basis of its acaricidal activity and facilitating its application in red spider mite biocontrol.

The mechanism of γ-T3-induced proliferation and differentiation of MC3T3-E1 cells via the activation of the Wnt/β-catenin signaling pathway by allowing the stabilization and nuclear translocation of β-catenin.

Purpose: To investigate the protective effect of mollugin on glucocorticoid (GC)-induced osteoporosis in rats. Methods: A total of 30 female Sprague Dawley rats (weighing 180 to 200 g) were randomly assigned to five groups of six rats each: control, GC and mollugin groups (20, 40 and 80 mg/kg, respectively). Except for the control group, osteoporosis was induced in the rats by intramuscular administration of dexamethasone at a dose of 2.5 mg/kg twice weekly for nine weeks. Bone mineral density (BMD) and serum activities of tartrate-resistant acid phosphatase (TRAP) and specific alkaline phosphatase (ALP), and levels of collagen type I fragment (CTX) and osteocalcin were estimated. The effect of mollugin alone, and in the presence of PI3K/Akt inhibitor on the proliferation of bone marrow osteoblasts was investigated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-tetrazolium bromide (MTT) assay. Western blotting was used for determination of the expressions of p-Akt, Akt and cyclin D1 protein. Results: There were significant increases in body weights of rats in GC group, when compared with the control group. However, treatment with mollugin significantly reduced the body weights in a dosedependent manner (p < 0.05). The BMD was significantly reduced in GC group, relative to the control group (p < 0.05). Serum activities of TRAP and ALP were significantly higher in GC group than in control group, but were significantly reduced by mollugin treatment (p < 0.05). Serum level of CTX was significantly increased and osteocalcin reduced in the GC group, relative to control (p < 0.05). Osteoblast proliferation was significantly higher in the mollugin-treated groups. The expressions of p-Akt, Akt and cyclin D1 were significantly and dose-dependently higher in mollugin-treated groups (p < 0.05). There were more viable osteoblasts in the mollugin-treated groups than in the untreated group. However, treatment with mollugin in the presence of PI3K/Akt inhibitor significantly reduced their viability (p < 0.05). Conclusion: Mollugin has therapeutic potential for GC-induced osteoporosis via mechanism involving the PI3K/Akt pathway.

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