Prevotella intermedia Aggravates Subclinical Hypothyroidism.

Subclinical hypothyroidism (SCH) has been shown to be associated with microbiota. However, the association between SCH and oral microbiota has not yet been elucidated. The results of our previous clinical studies showed that Prevotella intermedia was abundant in the oral microbiota of SCH patients. This study aimed to investigate the relationship between SCH and oral microbiota, verify the pathogenicity of P. intermedia in SCH, and preliminarily explore the possible mechanism. The SCH mouse model with oral application of P. intermedia was established, and the variance in the mouse oral microbiota and changes in thyroid function and metabolism were detected in mice. Student's t test and analysis of variance were used for statistical analysis. Oral application of P. intermedia changed the composition of the oral microbiota of SCH mice, which enhanced the damage to the thyroid and decreased the expression of functional genes of the thyroid. Moreover, P. intermedia decreased oxygen consumption and aggravated glucose and lipid metabolism disorders in SCH mice. Glucose tolerance and insulin tolerance decreased, and the triglyceride content of the liver and inflammatory infiltration in adipose tissue increased in SCH mice after P. intermedia stimulation. Mechanistically, P. intermedia increased the proportion of CD4+ T cells in cervical lymph nodes and thyroids in SCH mice. Th1 cells were suggested to play an important role in the pathogenesis of SCH involving P. intermedia. In conclusion, P. intermedia aggravated SCH manifestations, including thyroid dysfunction and glucose and lipid metabolism disorders, by causing immune imbalance in mice. This study sheds new light on the pathogenesis of SCH from the perspective of oral microbiota.

[Effects of heat shock pretreatment on the translocation and expression of alpha B-crystallin in cultured neonatal rat cardiomyocytes].

UNLABELLED: The effects of heat shock pretreatment on translocation and expression of alpha B-crystallin were evaluated in neonatal rat cardiomyocytes. RESULTS: 1. Western blot analysis demonstrated that cytosolic soluble alpha B-crystallin rapidly translocated to insoluble intracellular structure at 10 or 30 minutes and returned to cytosolic soluble compartment at about 1-2 h after heat shock. 2. Double staining of immunofluorescence showed that alpha B-crystallin redistributed in cytosol after heat shock, while HSC70 translocated from cytosol to nucleus. 3. Quantitative analysis with immunoelectronic microscopy demonstrated alpha B-crystallin translocated to cytoskeletal structure such as Z-line and nuclear envelope after heat shock. 4. Northern-blot showed that heat shock induced alpha B-crystallin mRNA expression. The rapid translocation and increasing expression of alpha B-crystallin after heat shock suggests that this small heat shock protein may play an important protective roles during the early and late phases of myocardial ischemic preconditioning.

[Heat shock pretreatment increases alpha B-crystallin expression and protects cardiomyocytes against injury induced by hydrogen peroxide].

The protective effects of heat shock pretreatment against the injury induced by hydrogen peroxide(H2O2) were evaluated in neonatal rat cardiomyocytes. The results showed that heat shock pretreatment significantly reduced cell mortality rate, LDH release rate and increased total antioxidation of the cells. Western blot analysis demonstrated that heat shock pretreatment induced expression of alpha B-crystallin and immunoelectron microscopy demonstrated H2O2-mediated alpha B-crystallin translocation from cytoplasm to nucleus and microfilament in cardiomyocytes. The results suggest that the mechanism of protective effect of heat shock pretreatment might involve the induction and translocation of alpha B-crystallin which then protect cardiomyocytes against H2O2-induced injury by stabilizing cytoskeletal structure and increasing anti-oxidation capacity of the cells.