Background. The aim was to develop a diagnostic questionnaire for damp phlegm pattern and blood stasis pattern in coronary heart disease patients (CHD-DPBSPQ). Methods. The standard procedures of questionnaire development were carried out to develop and assess CHD-DPBSPQ. The patients were assessed using the CHD-DPBSPQ, CHD-DPPQ, and CHD-BSPQ. Four methods were used to select the items on the CHD-DPBSPQ in a pilot study based on data from a Guizhou tertiary grade A hospital. Cronbach’s alpha and the split-half reliability, test-retest reliability, content validity, criterion validity, construct validity, and convergent validity were determined in a validation study using a nationwide sample. Results. After item selection, the CHD-DPBSPQ contained 15 items in two domains: the phlegm domain (9 items) and the blood stasis domain (6 items). For the CHD-DPBSPQ, the alpha coefficient was 0.88, the split-half coefficient was 0.90, and the intraclass correlation coefficient was 0.83. The range of the item-level content validity index (I-CVI) was 0.71 to 1.0 and that of the scale-level content validity index/average (Scale-CVI/Ave) was 0.97. The domain scores on the CHD-DPBSPQ were in close relation to the scores on a questionnaire for damp phlegm pattern in coronary heart disease patients (CHD-DPPQ) and a questionnaire for blood stasis pattern in coronary heart disease patient (CHD-BSPQ) (P<0.01). The root mean square error of approximation (RMSEA) was equal to 0.05 (90% CI: 0.044, 0.059). Convergent validity was demonstrated with a moderate correlation. Conclusion. The CHD-DPBSPQ is a reliable and valid instrument.
Objectives: The aim of this study was to establish a quantitative syndrome differentiation model with logistic regression analysis for phlegm and blood stasis syndrome (PBSS) in coronary heart disease (CHD) to offer methodology guidance for the quantitative syndrome differentiation of Traditional Chinese Medicine (TCM). Design: Tongue, face, and pulse information of each subject was obtained using the TCM-intelligent diagnosis instruments. Logistic regression model was used to construct the syndrome diagnosis model. The area under receiver operating characteristic curve (ROC-AUC) was used to evaluate the diagnostic value of the model. Subjects: Among the 141 subjects, 83 belonged to the PBSS group, and 58 belonged to the non-PBSS group. Results: The independent indexes used to predict PBSS in patients with CHD were length of the crack (LC) (p = 0.002), number of ecchymosis (NE) (p < 0.001), length of philtrum (LEP) (p = 0.022), and right hand pulse h1 (Rh 1) (p = 0.021). The expression of combining predictor L in this study was L = LC +57.58 NE +4.53 LEP +2.68 Rh 1. The ROC curve analysis indicated that the AUC values of LC, NE, LEP, and Rh 1 were 0.646, 0.710, 0.619, and 0.613, respectively. The AUC = 0.825 of the syndrome diagnosis model was the largest. Conclusions: The quantitative study of TCM syndrome based on logistic regression analysis provides a good method for the objective analysis and application of TCM syndrome.
Background. Hyperlipidemia, due to the practice of unhealthy lifestyles of modern people, has been a disturbance to a large portion of population worldwide. Recently, several scholars have turned their attention to Chinese medicine (CM) to seek out a lipid-lowering approach with high efficiency and low toxicity. This study aimed to explore the mechanism of Huatan Jiangzhuo decoction (HTJZD, a prescription of CM) in the treatment of hyperlipidemia and to determine the major regulation pathways and potential key targets involved in the treatment process. Methods. Data on the compounds of HTJZD, compound-related targets (C-T), and known disease-related targets (D-T) were collected from databases. The intersection targets (I-T) between C-T and D-T were filtered again to acquire the selected targets (S-T) according to the specific index. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, as well as network construction, were applied to predict the putative mechanisms of HTJZD in treating hyperlipidemia. Thereafter, an animal experiment was conducted to validate the therapeutic effect of HTJZD. In addition, regulated differentially expressed genes (DEGs) were processed from the RNA sequencing analysis results. Common genes found between regulated DEGs and S-T were analyzed by KEGG pathway enrichment to select the key targets. Lastly, key targets were validated by real-time quantitative reverse transcription PCR (qRT-PCR) analysis. Results. A total of 210 S-T were filtered out for enrichment analysis and network construction. The enrichment results showed that HTJZD may exert an effect on hyperlipidemia through the regulation of lipid metabolism and insulin resistance. The networks predict that the therapeutic effect of HTJZD may be based on the composite pharmacological action of these active compounds. The animal experiment results verify that HTJZD can inhibit dyslipidemia in rats with hyperlipidemia, suppress lipid accumulation in the liver, and reverse the expression of 202 DEGs, which presented an opposite trend in the model and HTJZD groups. Six targets were selected from the common targets between 210 S-T and 202 regulated DEGs, and the qRT-PCR results showed that HTJZD could effectively reverse Srebp-1c, Cyp3a9, and Insr mRNA expression (P < 0.01). Conclusion. In brief, network pharmacology predicted that HTJZD exerts a therapeutic effect on hyperlipidemia. The animal experimental results confirmed that HTJZD suppressed the pathological process induced by hyperlipidemia by regulating the expression of targets involved in lipid metabolism and insulin resistance.
In this paper, we present our study on the effect of atractylenolide II on hyperlipidemic model mice. After 8 weeks, the blood of these mice was taken to detect four lipids. Pathological changes were detected in the aortas and livers of the mice. Expression of PPARα and SREBP-1C was detected in the liver by western blot. An enzyme-linked immunosorbent assay was used to detect the effects of atractylenolide II on blood lipids in hyperlipidemia mice. Hematoxylin and eosin staining was used to detect pathological changes in the aortas and livers of mice with hyperlipidemia after treatment with atractylenolide II. Changes in PPARα and SREBP-1C expression were found in mice with dyslipidemia. As the results shown, atractylenolide II administration reduced body weight and hyperlipidemia in hyperlipidemic model mice. In addition, atractylenolide II effectively relieved fat deposition and damage in aortic and liver tissues. Therefore, atractylenolide II had a beneficial therapeutic effect in reducing hyperlipidemia in hyperlipidemic model mice, which may be related to its ability to inhibit SREBP-1C expression by activating PPARα. The molecular mechanism driving the therapeutic effect of atractylenolide II may involve upregulation of PPARα and activation of the AMPK/PPARα/SREBP-1C signaling pathway. Our research demonstrated the development of therapeutic agents that can be used to improve hyperlipidemia.
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