PDTC administration fails in transforming the suppressive influence of silibinin on p53 expression, indicating that the relationship between p53 and NF B is in a one waydirection. NF B has been recognized as a regulator of autophagy generally in most problems, while, the pro autophagic effect of NF W and the correspondent mechanisms are hardly noted. Our present study has showed that NF B inhibitor PDTC effectively inhibits silibinin caused autophagy. In addition, LPS, which will be able to cause irritation through causing Toll like receptors, price PF299804 induces NF B activation along with up handles autophagy, and this method can be abrogated by PDTC, suggesting that stimulating NF W activation both by silibinin or LPS induces autophagy in A375 S2 cells. Results from several other studies also provide ideas that it could have an optimistic legislation between autophagy and NF W. As an example, Delgado et al. Have discovered that autophagy also participates in adaptive immunity responses. Toll like receptors are activated and evoke autophagy in protecting extrinsic pathogen. In this Lymph node situation, autophagy increases the presentation of antigen peptide to MHC II, which facilitates the maturation of macrophages, encourages the proliferation and differentiation of T cells, and mediates inflammatory responses and all these characteristics of autophagy act like that of NF B activation. Therefore our findings as well as several other results show that under certain circumstances, NF W may function as a mediator of autophagy. Siwak et al. have found that reduction of NF T by curicumin facilitates cell apoptosis in human cancer cells. Thus, NF W activation mediated autophagy can be done to become a protective system in melanoma cells. And considering our formerly study about silibinins cyto protective influence against mitomycin C induced apoptosis in A375 S-2 cells, we examine the role of autophagy in controlling survival and cell death by using mitomycin C induced A375 S2 apoptosis design. As it happens that abrogation of natural product library autophagy with 3 MA somewhat abolishes silibinins suppressive effects on mitomycin C induced apoptosis. In yet another word, autophagy plays a professional survival part in silibinin antagonizing mitomycin C induced apoptosis. And this finding is in consistence with the study by Lester M. et al. Who’ve discovered that induction of autophagy enhances the cyto protective effect in UVA activated photosensitizer hypericin treated melanoma cells. In conclusion, in A375 S-2 cells it’s unearthed that silibinins suppressive influence on p53 expression helps NF B activation, and eventually mediates autophagy, which, represents a professional survival part in silibinin antagonizing mitomycin C induced apoptosis. More over, there’s a feedback loop between silibinin induced p53 and autophagy withdrawal dependent NF B activation.