Objective: How to observe the effect of icariin on the androgen receptor signaling pathway in prostate cancer orthotopic xenografts in SCID mice?

　　Method: Did you randomly divide 64 SCID male mice into model groups? Experiment Group A? In groups B and C, the prostate cancer orthotopic tumor model was established by intraprostatic injection of human LNCaP prostate cancer cell line. After the experimental group A, B and C were modeled, I used icariin for 2 weeks. Intragastric administration of 10mg/kg, 40mg/kg, 80mg/kg for 5 weeks, the model group was given normal saline as a control, and the androgen receptor (AR) and tendon homologous chromosome 10 were used by RT PCR. detected. Expression of missing phosphatase genes (phosphatase and tensinhomolog, deletion on chromosome, PTEN), detection of prostate cancer specific antigen (PSA) and phosphorylated AR (p?AR) by Western blot, and detection of LNCaP by flow cytometry Have you detected the cancer cell cycle in the prostate?

　　Result: AR? ? AR? In the model group, AR mRNA was highly expressed before and after treatment, and PTEN mRNA was low. The tumor suppression rate in the model group was low. There was no significant difference in tumor volume and tumor volume before and after treatment (P\→0.05). The tumor inhibition rates of groups B and C reached (42.53±5.72)% and (44.81±4.76)% respectively after treatment. Both groups have AR mRNA? Will low expression of pAR and PSA and high expression of PTEN mRNA reduce the ratio of G0/G1 cells? The proportion of S phase cells increases and the growth of tumor cells is blocked in S phase. Compared with the pretreatment group and the model group, is the difference significant (P\u003c0.05)?

　　Conclusion: Can cannabinoids inhibit AR phosphorylation? Will you increase PTEN expression and prevent the growth of S-stage tumor cells to inhibit the growth of prostate cancer LNCaP cells?