No abstract

This study explored the inhibiting effect and mechanism of myricanol on lung adenocarcinoma A549 xenografts in nude mice. Forty nude mice with subcutaneous A549 xenografts were randomly divided into five groups: high-dose myricanol (40 mg/kg body weight) group; middle-dose myricanol (20 mg/kg body weight) group; low-dose myricanol (10 mg/kg body weight) group; polyethylene glycol 400 vehicle group (1 mL/kg); and tumor model group. Nude mice were sacrificed after 14 days of treatment and the tumor inhibition rate (TIR, %) was then calculated. The relative mRNA expression levels of Bax, Bcl-2, VEGF, HIF-1α, and survivin in the tumor tissues were determined by real-time PCR. TUNEL assay was applied to determine cellular apoptosis, while IHC test was performed to detect the protein expression levels of Bax, Bcl-2, VEGF, HIF-1α, and survivin. The TIR of the three myricanol-treated groups ranged from 14.9% to 38.5%. The IHC results showed that the protein expression of Bcl-2, VEGF, HIF-1α, and survivin were consistently downregulated, whereas that of Bax was upregulated after myricanol treatment. Myricanol also significantly upregulated the mRNA expression of Bax and downregulated that of Bcl-2, VEGF, HIF-1α, and survivin in a dose-dependent manner (p < 0.05 to 0.001). These results are consistent with those of IHC. The TUNEL assay results indicated that apoptotic-positive cells significantly increased in the myricanol-treated tumor tissues compared with the cells of the vehicle control group (p < 0.01 to 0.001). These data suggest that myricanol could significantly decelerate tumor growth in vivo by inducing apoptosis.

BackgroundRecent studies have found that plant derived microRNA can cross-kingdom regulate the expression of genes in humans and other mammals, thereby resisting diseases. Can exogenous miRNAs cross the blood-prostate barrier and entry prostate then participate in prostate disease treatment?MethodsUsing HiSeq sequencing and RT-qPCR technology, we detected plant miRNAs that enriched in the prostates of rats among the normal group, BPH model group and rape bee pollen group. To forecast the functions of these miRNAs, the psRobot software and TargetFinder software were used to predict their candidate target genes in rat genome. The qRT-PCR technology was used to validate the expression of candidate target genes.ResultsPlant miR5338 was enriched in the posterior lobes of prostate gland of rats fed with rape bee pollen, which was accompanied by the improvement of BPH. Among the predicted target genes of miR5338, Mfn1 was significantly lower in posterior lobes of prostates of rats in the rape bee pollen group than control groups. Further experiments suggested that Mfn1 was highly related to BPH.ConclusionsThese results suggesting that plant-derived miR5338 may involve in treatment of rat BPH through inhibiting Mfn1 in prostate. These results will provide more evidence for plant miRNAs cross-kingdom regulation of animal gene, and will provide preliminary theoretical and experimental basis for development of rape bee pollen into innovative health care product or medicine for the treatment of BPH.Electronic supplementary materialThe online version of this article (10.1186/s12906-018-2107-y) contains supplementary material, which is available to authorized users.

No abstract

Background: Lung cancer is the leading cause of cancer-related mortality worldwide. Despite the new chemotherapy regimens and cytotoxic combinations investigated in multiple clinical trials in recent years, no significant improvement in the prognosis of patients with lung cancer has been achieved. Recently, scientists have focused on the potential role of extracts of traditional Chinese medicinal herbs as alternative and complementary medications for cancer treatment. Myricanone, a typical large ring of cyclic diarylheptanoids, is abundant in the bark of Myrica. Our studies have found that myricanone exerts potent anticancer activity. This study aimed to investigate the underlying mechanism of the effect of myricanone on A549 cells in vitro. Methods: A549 cells were treated with different concentrations of myricanone for the following assays. Tritiated thymidine incorporation was used to measure growth inhibition. Flow cytometry was used to detect apoptosis and cell cycle progression, and colony formation was performed to observe the effect of myricanone on the A549 proliferation rate. Results: Myricanone induced significant dose-dependent growth inhibitory effects on A549 cells with an IC₅₀ of 3.22 µg/ml. A significant decrease in colony formation was observed. This decrease induced cell apoptosis, G₁ phase arrest and the emergence of the sub-G₀ peak in A549 cells. Conclusions: These results suggest that myricanone exhibits anticancer activity and may be applicable in the clinical prevention and treatment of lung cancer in the future.