BackgroundThe present analysis was designed to investigate the association of type 2 diabetes (T2D) with high sensitivity cardiac troponin T (hs-cTnT) during the 5 years of follow-up, and explore which one of fasting blood glucose (FBG) and postprandial blood glucose (PBG) is a determinant of this association in Chinese community-dwelling population.MethodsThis prospective community-based analysis was conducted based on 730 participants without coronary artery disease and hs-cTnT values ≥14 pg/mL receiving two measurements of hs-cTnT levels at baseline and follow-up of 5 years.ResultsPrevalence of T2D was 16.2% (118 participants). Median hs-cTnT levels were 4 (3-7) pg/mL and 6 (5-9) pg/mL at baseline and follow-up, respectively. The variation in hs-cTnT levels had a median of 2 (0-4) pg/ml (p < 0.001 for variation), and incidence of hs-cTnT levels ≥14 pg/ml was 7.1% (52 participants) at follow-up. T2D had a significant association with elevated hs-cTnT levels in multivariate Logistic regression models (p < 0.05). Elevated levels of PBG (p < 0.05) rather than FBG (p > 0.05) determined the significant association with elevated hs-cTnT levels in multivariate linear regression models.ConclusionsThis community-based analysis observed that there was a significant increment of hs-cTnT levels, and baseline T2D had a significant association with elevated hs-cTnT levels during the 5 years of follow-up. Moreover, the present analysis demonstrated that PBG rather than FBG played a crucial role in this association in Chinese community-dwelling population without CAD.Electronic supplementary materialThe online version of this article (10.1186/s12986-017-0229-8) contains supplementary material, which is available to authorized users.
The effect of pachymic acid (PA) on pulmonary fibrosis in rats was expected to be investigated in this study. Firstly, bleomycin (BLM) was used to establish pulmonary fibrosis rat model, then PA (10, 20, or 40 mg/kg) was intragastrically administered to the rats for 14 days. Subsequently, a variety of tests was performed to observe changes in sample tissues after different treatments. Briefly, the degree of pulmonary edema in rats was assessed through dry/wet weight ratio. Hematoxylin and eosin (H&E) staining and Masson's trichrome staining were used to observe the pathological injury and fibrosis of lung tissue. Biochemical kits were applied to measure the levels of hydroxyproline (Hyp), transforming growth factor beta‐1 (TGFβ‐1), malondialdehyde (MDA), reactive oxygen species (ROS), and adenosine triphosphate (ATP) and the activities of superoxide dismutase (SOD) and catalase (CAT) in rat lung tissues of each group. The mitochondrial DNA (mtDNA) copy number in rat lung tissue was tested using qRT‐PCR. Additionally, the western blot was employed to detect the expression levels of pulmonary fibrosis‐related proteins and endoplasmic reticulum (ER) stress‐related proteins in each group of rat lung tissue. By virtue of experimental verification above, PA was discovered to alleviate BLM‐induced pulmonary edema, pulmonary fibrosis and histopathological damage. On the one hand, PA treatment decreased Hyp and TGF‐β1 levels and down‐regulated pulmonary fibrosis‐related protein expression [collagen I, α‐smooth muscle actin (α‐SMA), and fibronectin] in the lung tissue of BLM rats. On the other hand, it significantly increased the levels of SOD, CAT and ATP while decreased the activities of MDA and ROS in BLM rat lung tissues. In addition, the expression levels of ER stress‐related proteins [glucose‐regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), Caspase 9, and activating transcription factor 4 (ATF4)] were significantly down‐regulated in the lung tissue of BLM rats after PA treatment. Collectively, PA may ameliorate BLM‐induced pulmonary fibrosis and histopathological damage in rats through inhibiting ER stress and improving mitochondrial function.
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