In order to further confirm
these results, the examination of apoptosis related proteins was carried out. Bax and Bcl-2 as the early regulator of cell apoptosis and cytochrome c release [45], caspase-3 as the hallmark of apoptosis [46], and p53 as the regulator of cytochrome c release from mitochondria [47] were chosen as the representative proteins to analyze cell apoptosis upon exposed to AFB1, ST and their combinations. Immunocytochemistry was selected as the method since the distribution of apoptosis-related proteins have different locations in the cell, and the analysis of these proteins in a cell context can be used to validate the event of cell apoptosis as well as to observe morphological changes of cells upon exposure to mycotoxins. However, the optical density of the proteins learn more obtained though Omipalisib ic50 imaging analysis can only be used as a reference reflecting the trend of changes. In another word, the immunocytochemistry analysis is considered
as a semi-quantitative method to evaluate the relative changes of protein expressions. Mitochondria is an important player in cell apoptosis [45] with its apoptosis-associated BCL2 family proteins including Bax and Bcl-2. Bax promotes the release of cytochrome c [48] that is important to the activation of caspase cascade [49] while Bcl-2 is anti-apoptotic by regulating the activity of Bax. In normal cells, there exists a balance between these pro- and anti-apoptotic proteins, and a disruption of this balance often results in some pathological conditions such as human autosomal-dominant polycystic kidney disease with down-regulated Bcl-2 [50]. Thus the ratio of Bax and Bcl-2 might be more important to evaluate cell
Apoptosis [51]. In the current investigation, Bcl-2 showed a dose-dependent decrease of its content, and Bax, except the 10% dosage with an increased content, also showed a decreased expression compared to the control (Table 3). It looks like that both Bax and Bcl-2 from imaging analysis showed a decrease as the increase of the concentration of AFB1 and ST, but the ratio of Bax and Bcl-2 with a value from 1.37-2.88 in the treatment group is higher than the control group of 1.12, supporting the pro-apoptotic function of Bax and Bcl-2 to HepG2 cells upon exposed to mycotoxins. The decreased signal of Bax at high level Erythromycin exposure to mycotoxin is probably due to the degradation of Bax since the induced cytochrome c release by Bax is the earliest event occurred during cell apoptosis, and with high rate of cell apoptosis at high dosage (more dead cells at the later phase of apoptosis), the Bax protein might have been degraded by the caspase cascade leading to a decrease signal of Bax after 2-day treatment. As for Bcl-2, the decreased signal along the dosage might be caused by a lower expression of Bcl-2 as what has been shown in the literature [52]. The immunocytochemistry image (Fig.
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