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The precise cytotoxicity of  E. Adenophorum  in relation to the cell cycle and apoptosis of splenocytes in Saanen goats remains unclear. In the present study, 16 Saanen goats were randomly divided into four groups, which were fed on 0%, 40%, 60% and 80%  E. adenophorum  diets. The results of TUNEL, DAPI and AO/EB staining, flow cytometry analysis and DNA fragmentation assays showed that  E. adenophorum  induced typical apoptotic features in splenocytes, suppressed splenocyte viability, and caused cell cycle arrest in a dose-dependent manner. However, westernblot, ELISA, qRT-PCR and caspase activity analyses showed that  E. adenophorum inhibited Bcl-2 expression, promoted Bax translocation to the mitochondria, triggered the release of Cyt c  from the mitochondria into the cytosol, and activated caspase-9 and -3 and the subsequent cleavage of PARP. Moreover, in  E. adenophorum -induced apoptosis, the protein levels of Fas, Bid, FasL and caspase-8 showed no significant changes.  E. adenophorum  treatment induced the collapse of  ΔΨ m. Moreover, these data suggested that  E. adenophorum  induces splenocyte apoptosis via the activation of the mitochondrial apoptosis pathway in splenocytes. These findings provide new insights into the mechanisms underlying the effects of  E. adenophorum  cytotoxicity on splenocytes.

E. adenophorum induces Cell Cycle Arrest and Apoptosis of Splenocytes through the Mitochondrial Pathway and Caspase Activation in Saanen Goats