Objective:To investigate the role of pyroptosis in T-2 toxin induced articular cartilage injury.Methods:A total of 145 SPF grade male Wistar rats were randomly divided into blank control group ( n = 45), solvent control group ( n = 45), and T-2 toxin group ( n = 55) based on body weight (50 - 70 g). The T-2 toxin group and the solvent control group were given 100 ng·g -1·d -1 T-2 toxin and an equal amount of anhydrous ethanol by gavage, respectively; the blank control group was fed routinely. Fifteen rats from each group were euthanized at 6, 12, and 24 weeks of intervention, and bilateral knee joints of the rats were collected. Pathological changes in rat knee articular cartilage were observed using hematoxylin and eosin staining. TdT-mediated dUTP nick-end labeling (TUNEL) staining was used to detect chondrocyte injury. Western blot was used to detect the protein expression of gasdermin D (GSDMD), cleaved N-terminal of gasdermin D (GSDMD-N), NOD like receptor thermal protein domain associated protein 3 (NLRP3), cysteinyl aspartate specific proteinase 1 (Caspase-1), interleukin 1β (IL-1β), interleukin 18 (IL-18), and apoptosis-associated spike-like protein containing CARD (ASC). Results:At 6, 12, and 24 weeks of intervention, the T-2 toxin group rats showed varying degrees of damage to the knee articular cartilage tissue, including a decrease in the number of chondrocytes and death. At 24 weeks of intervention, the TUNEL staining positivity rates of chondrocytes in the blank control group, solvent control group, and T-2 toxin group were (1.28 ± 0.45)%, (0.73 ± 0.27)%, and (4.01 ± 2.37)%, respectively, with statistically significant differences between the groups ( F = 6.11, P = 0.036); and the T-2 toxin group was higher than the blank control group ( P < 0.05). At 24 weeks of intervention, there were statistically significant differences in the expression levels of NLRP3, Caspase-1, GSDMD, GSDMD-N, and IL-1β proteins among the blank control group, solvent control group, and T-2 toxin group ( F = 3.81, 11.81, 6.74, 3.71, 155.49, P = 0.044, 0.003, 0.023, 0.036, 0.001); and the T-2 toxin group was higher than the blank control group ( P < 0.05). At different intervention cycles, there was no statistically significant difference in the expression levels of ASC and IL-18 proteins among the groups ( F = 0.78, 0.93, 3.73, 2.26, 0.88, 0.11, P > 0.05). Conclusion:The NLRP3/Caspase-1/GSDMD pathway mediated pyroptosis is involved in T-2 toxin induced articular cartilage injury in rats.

Objective:To investigate the role of pyroptosis in T-2 toxin induced articular cartilage injury.Methods:A total of 145 SPF grade male Wistar rats were randomly divided into blank control group ( n = 45), solvent control group ( n = 45), and T-2 toxin group ( n = 55) based on body weight (50 - 70 g). The T-2 toxin group and the solvent control group were given 100 ng·g -1·d -1 T-2 toxin and an equal amount of anhydrous ethanol by gavage, respectively; the blank control group was fed routinely. Fifteen rats from each group were euthanized at 6, 12, and 24 weeks of intervention, and bilateral knee joints of the rats were collected. Pathological changes in rat knee articular cartilage were observed using hematoxylin and eosin staining. TdT-mediated dUTP nick-end labeling (TUNEL) staining was used to detect chondrocyte injury. Western blot was used to detect the protein expression of gasdermin D (GSDMD), cleaved N-terminal of gasdermin D (GSDMD-N), NOD like receptor thermal protein domain associated protein 3 (NLRP3), cysteinyl aspartate specific proteinase 1 (Caspase-1), interleukin 1β (IL-1β), interleukin 18 (IL-18), and apoptosis-associated spike-like protein containing CARD (ASC). Results:At 6, 12, and 24 weeks of intervention, the T-2 toxin group rats showed varying degrees of damage to the knee articular cartilage tissue, including a decrease in the number of chondrocytes and death. At 24 weeks of intervention, the TUNEL staining positivity rates of chondrocytes in the blank control group, solvent control group, and T-2 toxin group were (1.28 ± 0.45)%, (0.73 ± 0.27)%, and (4.01 ± 2.37)%, respectively, with statistically significant differences between the groups ( F = 6.11, P = 0.036); and the T-2 toxin group was higher than the blank control group ( P < 0.05). At 24 weeks of intervention, there were statistically significant differences in the expression levels of NLRP3, Caspase-1, GSDMD, GSDMD-N, and IL-1β proteins among the blank control group, solvent control group, and T-2 toxin group ( F = 3.81, 11.81, 6.74, 3.71, 155.49, P = 0.044, 0.003, 0.023, 0.036, 0.001); and the T-2 toxin group was higher than the blank control group ( P < 0.05). At different intervention cycles, there was no statistically significant difference in the expression levels of ASC and IL-18 proteins among the groups ( F = 0.78, 0.93, 3.73, 2.26, 0.88, 0.11, P > 0.05). Conclusion:The NLRP3/Caspase-1/GSDMD pathway mediated pyroptosis is involved in T-2 toxin induced articular cartilage injury in rats.