I think you will not be unfamiliar with paclitaxel, because paclitaxel is a hot drug for cancer treatment in recent years. Paclitaxel drugs are widely used in clinical anti-tumor drugs. Docetaxel is the second generation product of paclitaxel family, which is used as a second-line anti-cancer drug for the treatment of prostate cancer. Studies have shown that nf- κ B is constitutively overexpressed in prostate cancer cells, and docetaxel further activates nf- κ B pathway in prostate cancer cells, resulting in tumor resistance to docetaxel. Therefore, finding an effective way to overcome the further activation of endogenous nf- κ B pathway by docetaxel will help to enhance the apoptosis effect induced by docetaxel, which is expected to enhance its clinical efficacy.

    Previous studies have shown that triptolide, a monomer of traditional Chinese medicine Tripterygium wilfordii, can inhibit the activity of proteasome, cause the accumulation of nf- κ B inhibitor I κ b- α, and then inhibit the nf- κ B pathway. In view of this, it is of great significance to study whether the combination of Tripterygium Wilfordii and docetaxel can reduce the activation of nf- κ B by docetaxel in prostate cancer cells, and then enhance the apoptosis effect induced by docetaxel. In some studies, human prostate cancer PC-3 cells were used as a model. MTT method confirmed that Triptolide and docetaxel alone inhibited the proliferation of prostate cancer cells in a dose-dependent manner. It was found that Triptolide and docetaxel could act synergistically. The results of flow cytometry showed that the proportion of apoptotic tumor cells was significantly increased in the combination of the two drugs compared with that in the single drug, showing more obvious morphological changes of apoptosis. It was further confirmed that the simultaneous treatment of triptolide and docetaxel could reduce the expression of nf- κ b/p65 at mRNA and protein levels, and inhibit the translocation of nf- κ b/p65 from cytoplasm to nucleus. It was also confirmed that triptolide inhibited the function of nf- κ B. Triptolide induced the accumulation of I κ b- α in cytoplasm, which may be related to triptolide inhibiting the function of nf- κ B. A series of results showed that Tripterygium Wilfordii and docetaxel had a synergistic effect on the proliferation of prostate cancer cells at low drug concentration, and the combination of Tripterygium Wilfordii and docetaxel resulted in a more extensive apoptosis. Triptolide inhibits the function of nf- κ B and reduces the induction of apoptosis protein nf- κ B by docetaxel, which may be one of the reasons why triptolide cooperates with docetaxel.

    Experiments show thatTriptolideIt has synergistic effect with docetaxel and has better therapeutic effect on prostate cancer.