AIM:To observe the effect of B-HT933, a selective α2-adrenoceptor agonist, on lipopolysaccha-ride ( LPS )-induced TNF-αproduction in neonatal rat cardiomyocytes and to explore the underlying mechanisms . METHODS:The neonatal rat cardiomyocytes were cultured .The localization of α2A-adrenoceptor in the cardiomyocytes was examined by immunofluorescence staining .The cardiomyocytes were exposed to LPS or/and B-HT933 for different time.The level of TNF-αin the supernatants and the mRNA expression of TNF-αwere detected by ELISA and real-time PCR, respectively.In addition, LPS-associated signal molecules in the cardiomyocytes were also examined by Western blotting.RESULTS: Immunofluorescence staining showed that α2A-adrenoceptors were localized in the cardiomyocytes . LPS stimulated TNF-αproduction in the cardiomyocytes in a dose and time-dependent manner .B-HT933 pretreatment sig-nificantly inhibited the expression of TNF-αat mRNA and protein levels in LPS-treated cardiomyocytes .Furthermore, LPS exposure induced IκBαand p38 phosphorylation in cardiomyocytes and only IκBαphosphorylation was prevented by B-HT933 treatment.CONCLUSION:α2A-adrenoceptors are present in neonatal rat cardiomyocytes and its agonist B -HT933 inhibits LPS-induced TNF-αproduction in cardiomyocytes via suppressing IκBαphosphorylation .

Objective:To explore the changes in the expression of Tau protein and phosphorylated Tau (p-Tau) protein in neurons after spinal cord ischemia-reperfusion injury (SCII).Methods:Ninety-six healthy adult SD rats were randomly divided into a sham operation group ( n=48) and a SCII group ( n=48). Based on the reperfusion time of 3 h, 6 h, 12 h, 24 h, 48 h and 72 h, the SCII group was divided into 6 subgroups ( n=8 per subgroup). Immunohistochemical staining was used to observe the apoptosis of spinal cord neurons in the L 4-L 5 segments and the expression of Tau protein and p-Tau protein. Results:In the sham operation group, the neuron cells were intact, mainly concentrated in the gray matter. Tau protein was seen in a small number of neuron cells, and a small amount of filamentous p-Tau protein in the pernucleus and cytoplasm. There was no significant difference between Tau protein and p-Tau protein expression in neurons at each time point ( P>0.05). In the SCII group, scattered Tau protein was seen in the apoptotic cells while there was a strong positive expression of Tau protein in the non-apoptotic cells. The expression of Tau protein in the SCII group gradually increased after injury, reaching a peak at 48h and plateauing at 72 h, and was significantly different between any 2 time points (except for 72 h) ( P<0.05). In the SCII group, the positive expression of p-Tau protein was observed in the cytoplasm of the apoptotic cells in strips and sheets. It increased rapidly within 6 h but did not change significantly after 6 h, showing no significant difference between any 2 time points afterwards ( P>0.05). There was a statistically significant difference in the expression of Tau protein and p-Tau protein between the SCII group and the sham operation group at each time point ( P<0.05). Conclusion:It is hopeful to reduce the severity of spinal cord injury by regulating the expression of Tau protein and p-Tau protein within 6 to 48 hours after SCII.