[Gualou Xiebai Banxia Decoction treats type 2 diabetes mellitus combined with acute myocardial infarction via chemerin/ CMKLR1/PPARα signaling pathway].

This study aims to investigate the effects of Gualou Xiebai Banxia Decoction(GXBD) on type 2 diabetes mellitus(T2DM) combined with acute myocardial infarction(AMI) in rats via chemerin/chemokine-like receptor 1(CMKLR1)/peroxisome proliferator-activated receptor α(PPARα) signaling pathway, and to explore the mechanism of GXBD in alleviating glucose and lipid metabolism disorders. The SD rats were randomized into control, model, positive control, and low-and high-dose GXBD groups. The rat model of T2DM was established by administration with high-fat emulsion(HFE) by gavage and intraperitoneal injection with streptozotocin, and then coronary artery ligation was performed to induce AMI. The control and model groups were administrated with the equal volume of normal saline, and other groups were administrated with corresponding drugs by gavage. Changes in relevant metabolic indicators were assessed by ELISA and biochemical assays, and the protein levels of chemerin, CMKLR1, and PPARα in the liver, abdominal fat, and heart were determined by Western blot. The results showed that GXBD alleviated the myocardial damage and reduced the levels of blood lipids, myocardial enzymes, and inflammatory cytokines, while it did not lead to significant changes in blood glucose. Compared with the model group, GXBD down-regulated the expression of chemerin in peripheral blood and up-regulated the expression of cyclic adenosine monophosphate(cAMP) and protein kinase A(PKA) in the liver. After treatment with GXBD, the protein levels of chemerin and CMKLR1 in the liver, abdominal fat, and heart were down-regulated, while the protein levels of PPARα in the liver and abdominal fat were up-regulated. In conclusion, GXBD significantly ameliorated the disorders of glycolipid metabolism in the T2DM-AMI model by regulating the chemerin/CMKLR1/PPARα signaling pathway to exert a protective effect on the damaged myocardium. This study provides a theoretical basis for further clinical study of GXBD against T2DM-AMI and is a manifestation of TCM treatment of phlegm and turbidity causing obstruction at the protein level.

Gualou-Xiebai-Banxia decoction protects against type II diabetes with acute myocardial ischemia by attenuating oxidative stress and apoptosis via PI3K/Akt/eNOS signaling.

Gualou-Xiebai-Banxia decoction has a long history of medical use for treating cardiovascular diseases in China. In this study, we investigated the protective effect and underlying mechanisms GXB in type II diabetes with acute myocardial ischemia (T2DM-AMI) rats. We hypothesized that GXB may display its protective effect on T2DM-AMI by reducing endothelial progenitor cells (EPCs) apoptosisviaactivating PI3K (phosphatidyl inositol 3-kinase)/Akt (serine/threonine protein kinase B)/eNOS (endothelial nitric oxide synthase) signaling. Rats were challenged with a high-fat diet and intraperitoneal injection of streptozotocin to induce a model of type II diabetes mellitus (T2DM) and coronary ligation to induce acute myocardial infarction (AMI). Changes in metabolites were assessed via enzyme-linked immunoassay and biochemical examination. The number and apoptosis rate of EPCs in peripheral blood were detected by flow cytometry. Target mRNAs and proteins in EPCs were analyzed by RT-PCR and Western blot analysis. The results demonstrated that GXB treatment decreased T2DM-AMI-associated changes in plasma fasting blood glucose, muscular enzymes, and blood lipids, and reduced oxidative stress. Furthermore, EPC apoptosis was increased in T2DM-AMI rats and was associated with decreased mRNA and protein levels of PI3K, Akt, and eNOS compared to the controls. Conversely, T2DM-AMI rats treated with GXB exhibited more circulating EPCs and downregulated levels of cell apoptosis, combined with increased mRNA and protein levels of PI3K, Akt, and eNOS compared to those of untreated T2DM-AMI rats. Our study showed that GXB treatment mitigated EPC apoptosis and promoted PI3K/Akt/eNOS signaling in T2DM-AMI rats.

Anti-inflammatory effect of the compounds from the flowers of Trollius chinensis.

In order to investigate the anti-inflammatory activity of flavonoids, phenolic acids, and alkaloids from the flowers of Trollius chinensis, some representative compounds, namely, orientin, 2"-O-ß-L-galactopyranosylorientin, vitexin, quercetin, isoquercetin, luteolin, veratric acid, proglobeflowery acid, trollioside, and trolline were selected to study their inhibitory effects against LPS-induced NO, IL-6, and TNF-ß release in RAW264.7 cells. At the higher concentration, both phenolic acids and flavonoids inhibited the production of NO, whereas only phenolic acids showed this effect at the lower concentration. Although trolline had stronger cytotoxicity, it exhibited a potential effect of decreasing NO production induced by LPS in the non-toxic concentration range. In addition, all tested compounds decreased the production of IL-6 and TNF-a by almost 50% at both the higher and lower concentrations. It is concluded that the anti-inflammatory activity of the phenolic acids is stronger than that of the flavonoids.

Hepatic metabolism: a key component of herbal drugs research.

Liver is the largest metabolic organ for a wide range of endogenous and exogenous compounds and plays a crucial part in the pharmacokinetics and pharmacodynamics through various metabolic reactions. This review provides a progressive description of hepatic metabolism of herbal drugs with respect to metabolic types and investigational methods. In addition, the problems encountered during the research process are discussed.

Roles of Chinese medicine bioactive ingredients in the regulation of cellular function of endothelial progenitor cells.

To improve the function of endothelial progenitor cells (EPCs) is one of the goals in Chinese traditional therapy to treat various cardio-celebrovascular diseases. In the past decades, scholars in the field of traditional Chinese medicine (TCM) have found fifteen active compounds to regulate the function of EPC. These metabolites are extracted from thirteen, plant-based Chinese medicine, with majority of them as potent reductive or oxidative hydrophilic molecules containing phenyl groups. These active compounds either enhance the mobilization of EPC, or inhibit their apoptosis through different signaling pathways. In this review, the molecular structure, biophysical properties, and the plant sources of these active ingredients and their regulatory effects on the function of EPC are summarized, aiming to reveal the modern basis of Chinese medicine for promoting blood circulation and removing blood stasis at the progenitor cell level.

Salvianic acid A inhibits lipopolysaccharide-induced apoptosis through regulating glutathione peroxidase activity and malondialdehyde level in vascular endothelial cells.

AIM: To find out the role of salvianic acid A (SAA) in the protection of vascular endothelial cells (VEC) and its possible mechanism in vitro. METHODS: The ingredient at various concentrations was added to human umbilical vein endothelial cells (HUVEC) treated with 0.5 µmol·L(-1) lipopolysaccharide (LPS) for 24 h. Apoptotic morphological changes of cells were observed under inverted phase contrast microscope; the cell viability was quantified using MTT assay. Nuclear fragmentation of cells was observed under laser scanning confocal microcope after being stained with acridinorange. Cell cycle distribution was detected by flow-cytometry after being stained with propidium iodide (PI). The activities of glutathione peroxidase (GPH-PX) as well as maleic dialdehyde (MDA) level in cells were measured by spectrophotometric methods as described in the assay kits. RESULTS: Apoptotic morphological changes and the decrease of cell viability of these cells were obviously inhibited by SAA in a dose-dependent manner. Furthermore, the abnormal cell cycle distribution, the decrease of GSH-Px activity and the increase of MDA level induced by LPS were markedly reversed. CONCLUSION: SAA exerts protective effect on VEC induced by LPS via an antioxidative mechanism.