more NK cells activated, the more the rate of survival increased: 54% with the group of patients taking RBAC and 36% for the group without RBAC.
Numerous functions of RBAC (14) include improving the ratio of Bax/Bcl2 to increase the death of cancer cells, activation of caspases 3-8-9 and the induction of apoptosis. Bax is a tumor suppressor gene while BcL2 is an anti-apoptotic protein that increases cancer cell resistance during chemotherapy. In a study using RBAC to enhance radiotherapy in animals bearing Ehrlich ascites carcinoma, it was determined by which mechanism RBAC enhances the apoptotic effects of fractionated radiation. The expression levels of the apoptotic effects were evaluated showing a significant up-regulation in expression for P53, Bax and caspase 3, along with a significant decrease for BcL2 protein expression. Radiation exposure enhanced P53 and Bax expression by 58.8 and 43.4% respectively, while BcL2 expression decreased by 36.4% relative to the inoculated control group. In contrast, treatment with RBAC and radiation further increased up-regulation of P53 and Bax expression by 284.9% and 244.1% respectively, where BcL2 expression was markedly suppressed by 95.4% relative to the inoculated control group (15).
Figure 4: RBAC & Chemotherapy Compared to RBAC Alone