IPEC-J2

Toxic Effect of T-2 toxin on IPEC-J2 Cells

T-2 toxin, a prevalent mycotoxin in food and feed, poses significant risks to health through intestinal damage, which is not fully understood mechanistically. The MAPK signaling pathway, including pathways via JNK, ERK, and p38, regulates stress responses and inflammation. Using the IPEC-J2 cell line, Chen's team investigated whether T-2 toxin activates these pathways, particularly focusing on JNK, to induce oxidative stress and inflammation.

Using the CCK-8 method to examine the toxicity of T-2 toxin on IPEC-J2 cells, they first noted the impact of T-2 toxin on IPEC-J2 cell survival. In accordance with Fig. 1A, in contrast to the 0 ng/mL group, T-2 toxin had a substantial inhibitory impact on IPEC-J2 viability when the dose was more than 2 ng/mL. Therefore, T-2 toxin concentrations of 0, 1, 2, and 4 ng/mL were chosen for the follow-up studies. Further study showed that the LDH release significantly increased with the rose T-2 toxin treatment concentration (Fig. 1B). When IPEC-J2 cells were handle with T-2 toxin in contrast to untreated cells, the morphology changed, the intercellular space became larger, and the number decreased (Fig. 1C). These findings demonstrated that the T-2 toxin was toxic to IPEC-J2 cells.

Fig. 1. Toxic effect of T-2 toxin on IPEC-J2 cells (Chen FJ, Wang YH, et al., 2023).

Protective Effect of Genistein on Cell Viability and Intracellular ROS Levels on IPEC-J2 cells

Interest in natural feed additives for animal health has increased, focusing on genistein, a soybean isoflavone aglycone with strong antioxidant properties. While promising for pig intestinal health, its mechanism against oxidative stress was unclear. Li's team used the hydrogen peroxide-stimulated IPEC-J2 cells oxidative stress model was employed to explore the antioxidant capacity of genistein and potential mechanisms.

As revealed in Figure 2, cell viability was significantly reduced from 100% to 69.8% in the H₂O₂-treated group compared to the control group. However, in contrast to the H₂O₂-treated group, pretreating cells with 10, 20, and 40 μM genistein before H₂O₂ exposure enhanced cell viability from 69.8% to 83.8%, 86.5%, and 83.2%, respectively. For subsequent experiments, we opted for a concentration of 20 μM genistein as it exhibited enhanced cell viability at this particular dosage. As demonstrated in Figure 3, a significant elevation in intracellular ROS levels was observed in the H₂O₂-treated group compared to the control group. In contrast to the H₂O₂-treated group, pretreating cells with 20 μM genistein before H₂O₂ exposure showed a tendency to reduce intracellular ROS levels. Comparatively, the genistein treated group did not have elevated intracellular ROS levels.

Fig. 2. Effect of genistein on the IPEC-J2 cells viability (Li Y, Cai L, et al., 2024).

Fig. 3. Effect of genistein on ROS levels in IPEC-J2 cells (Li Y, Cai L, et al., 2024).