Abstract
In this report, we have investigated the apoptosis and autophagy of chondrocytes induced by the T-2 and HT-2 toxins. The viability of chondrocytes was measured by the MTT assay. Malondialdehyde (MDA) and superoxide dismutase (SOD) kits were used to measure the oxidative stress of chondrocytes. The apoptosis of chondrocytes was measured using flow cytometry. Hoechst 33258 and MDC staining agents were introduced to analyze apoptosis and autophagy induction in chondrocytes, respectively. Protein expression of Bax, caspase-9, caspase-3, and Beclin1 was examined by western blotting analysis. The T-2 and HT-2 toxins significantly decreased the viability of chondrocytes in a time-dependent manner. The level of oxidative stress in chondrocytes induced by the T-2 toxin was significantly higher when compared with that of the HT-2 toxin. The apoptosis rate of chondrocytes induced by the T-2 toxin increased from 3.26 ± 1.03%, 18.38 ± 1.28%, 34.5 ± 1.40% to 49.67 ± 5.31%, whereas apoptosis rate of chondrocytes induced by the HT-2 toxin increased from 3.82 ± 1.03%, 11.61 ± 1.27%, 25.72 ± 2.95% to 36.28 ± 2.81% in 48 h incubation time. Hoechst 33258 staining confirmed that apoptosis of chondrocytes induced by the T-2 toxin was significantly higher than that observed when the chondrocytes were incubated with the HT-2 toxin. MDC staining revealed that the autophagy rate of chondrocytes induced by the T-2 toxin increased from 6.38% to 63.02%, whereas this rate induced by the HT-2 toxin changed from 6.08% to 53.33%. The expression levels of apoptosis and autophagy related proteins, Bax, caspase-9, caspase-3, and Beclin1 in chondrocytes induced by the T-2 toxin were significantly higher when compared with those levels induced by the HT-2 toxin.
Highlights
Kashin–Beck disease (KBD) is an endemic, chronic, and deformed osteoarthropathic disease.There are 0.64 million KBD patients distributed from northeast to southwest regions of China.KBD patients suffer from joint pain, morning stiffness, limited motion, and joint enlargement [1,2].Three underlying risk factors are considered to be responsible for KBD: mycotoxin (T-2 toxin) in grain, selenium deficiency, and organic acid in drinking water [3,4]
Flow cytometry was used to analyze apoptosis of chondrocytes induced by the T-2 and HT-2 toxins incubation period, the apoptosis of chondrocytes induced by the T-2 toxin was significantly higher
At the same dose from 3.94% to 60.67%, whereas the apoptosis rate of chondrocytes incubated with the HT-2 toxin and incubation period, the apoptosis of chondrocytes induced by the T-2 toxin was significantly higher increased from 3.74% to 40.75%
Summary
Kashin–Beck disease (KBD) is an endemic, chronic, and deformed osteoarthropathic disease. T-2detected toxin detected in can grains can be converted rapidly converted the HT-2 toxin after the contaminated food. T-2 toxin rapidly combines proteins the and to is organs through the mouth, and respiratory [8]. T-2 toxin is metabolized to the HT-2 delivered to organs throughskin, the mouth, skin, andtract respiratory [8]. The. T-2 toxin is metabolized toxin the liver entering enterohepatic circulation. The Metabolism of the toxin to the toxin in to the liver and digestive from the 0 tosame. The toxic effects human chondrocytes remainchondrocytes poorly understood. Of the HT-2 toxin on human remain poorly understood. In this this study, study, human humanchondrocytes chondrocyteswere werecultured cultured bovine serum media.
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