The proliferation of vascular smooth muscle cells (VSMCs) is a key pathogenic characteristic of vascular remodeling diseases. The signal transducers and activators of transcription-3 (STAT3) signaling pathway is crucial for VSMCs growth, and its role in cytokine-induced VSMCs proliferation, calcification, and phenotypic switching is essential for developing new treatment targets. VSMCs can transform from contractile to synthetic phenotypes in response to stimuli, such as mechanical forces, growth factors, pro-inflammatory cytokines, and vascular injury. Understanding the mechanism of VSMCs proliferation triggered by the STAT3 pathway is important for identifying potential therapeutic targets for vascular remodeling diseases.
This study analyzed the synergistic development of the Traditional Chinese Medicine (TCM) service trade within the Greater Bay Area (GBA) in China, aiming to provide suggestions and references for the development of TCM service trade around the world.
Taking the typical and representative Guangdong, Hong Kong and Macao Greater Bay Area as the research object, this paper focused on four modes of “cross-border supply, offshore consumption, commercial presence, and movement of natural persons”, and explored the current situation of TCM service trade from four macroscopic aspects: political, economic, social, and technological, through case studies. The challenges in the development of TCM service trade were analyzed.
Our study found that the degree of synergistic openness of Guangdong, Hong Kong and Macao needs to be improved. The integration of trade in TCM services is the integration of TCM services with tourism. However, there is a relative lack of human resources in TCM in Hong Kong and Macao, with weak competitiveness of service bases. The resources of TCM services are still under-utilized, and the GBA market of TCM services lacks momentum.
We have come to the conclusion that the GBA need to promptly improve the unified standard system of TCM service trade. Actively building cultivating a “Bay Area GBA brand” for TCM service trade, steadily building a social climate in support of TCM service trade and vigorously promote the development of TCM service trade through digital technology, thus promoting the synergistic development of TCM service trade within the GBA.
Ulcerative colitis (UC) is a non-specific inflammatory bowel disease that has a high rate of recurrence, development of novel therapeutic approaches with high efficacy and few adverse effects are still needed. Dioscoreae persimilis is an edible plant that has been widely consumed as a remedy for gastrointestinal diseases in traditional Chinese medicine. Polysaccharides have been proven to have protective effects on UC. However, the role of polysaccharides from D. persimilis in UC has not been studied yet. The refined D. persimilis Polysaccharide (DP), which consists of glucose and galactose, was extracted and purified using three-phase partitioning (TPP) method. The primary chemical and structural characteristics of DP were investigated by UV, FT-IR, molecular weight, and monosaccharide composition. Based on dextran sulfate sodium (DSS) induced UC in mice, the alleviatory effect of DP on UC was explored. DP was found to alleviate histopathological changes of colon, improve colonic antioxidant capacity and ameliorate inflammation response in colitis mice. Moreover, 16S rDNA sequencing of fecal revealed that DP could restore the diversity and composition of gut microbiota, especially up-regulates the abundance of Acetatifactor, Lachnospiraceae, and Lactobacillus, and increase the ratio of Firmicutes/Bacteroidetes. According to this study, DP has the potential to serve as an effective nutritional supplement for improving colitis.
Tianhuang Formula (THF) is a hospital formula summarized by Professor Jiao Guo's 30 years of clinical experience. Some studies have shown that it can alleviate dyslipidemia in the body. The purpose of this study is to confirm whether THF can improve non-alcoholic fatty liver diseases (NAFLD) in type 2 diabetic mice induced by high-fat diet (HFD)/streptomycin (STZ) and to clarify its potential mechanism.
After induction of diabetes, mice were administrated with THF (60 mg/kg or 120 mg/kg) once daily for 10 weeks. Blood glucose (FBG), glucose tolerance, and insulin resistance (IR) were assayed by oral glucose tolerance test (OGTT) and insulin tolerance test (ITT). Blood lipids, alanine transaminase (ALT), and aspartate transaminases (AST) were detected. Serum fasting insulin (INS) and adiponectin (APN) levels were measured using ELISA. Histological changes in liver and pancreatic islets were observed by H&E staining, followed by Oil Red O staining for liver lipid quantification and periodic acid-Schiff (PAS) staining to detect glycogen accumulation. Western blotting detected the levels of fatty cardiolipin synthase 1 (CRLS1), transcription factor activator 3 (ATF3), and carbohydrate-responsive element binding protein (ChREBP) in the liver. The mRNA transcripts of hepatic inflammatory factors, lipogenesis and lipolysis-related genes, and gluconeogenic enzyme-phosphoenolpyruvate carboxykinase (PEPCK), CRLS1, ATF3, and ChREBP mRNA levels were evaluated by RT-qPCR.
THF restored impaired glucose tolerance and insulin resistance, respectively. There was an improvement in HFD/STZ-induced liver and islet damage, high serum HDL-C and ANP levels, and a significant decrease in FBG, total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), FFA, INS, ALT, and AST, and lipid droplet counts in the T2DM mice treated with THF. CREBBP binding protein ATF3 mediated the insulin resistance signaling pathway, which regulated glucose and lipid metabolism in the liver. THF upregulated CRLS1, and ChREBP downregulated the expression of downstream ATF3 in the liver. RT-qPCR analysis also systemically indicated that THF suppressed the pathway and key regulators related to inflammation, lipid accumulation, and gluconeogenesis.
Our findings demonstrated that THF ameliorated lipid profile and attenuated liver steatosis in T2DM mice through CRLS1-ATF3/ChREBP pathway activation.