Abstract
Metabolic syndrome (MetS) is a pathological state of metabolic disorders that primarily occur in human proteins, fats, and carbohydrates. It is a complex cluster of core metabolic disorder syndromes including obesity, hyperglycemia, dyslipidemia, and hypertension, and vascular endothelial injury, occurring over time. The currently available treatment options cannot effectively manage MetS. In our previous research, we revealed ChaiQi decoction (CQD) as an effective prescription for improving MetS; however, the specific mechanism remains unclear. Herein, we assessed the efficacy and mechanism of CQD in ApoE gene knockout (ApoE-) mice. Mice were administered with CQD daily for 12 weeks, and the measurement of their body weight was taken monthly. To evaluate the metabolic levels of mice, we determined the fasting blood glucose (FBG), fasting serum insulin (FINS), insulin resistance index (IRI), triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels. Furthermore, immunohistochemical analysis was adopted to determine the expression of ICAM-1 and VCAM-1 in vascular endothelium, while an optical microscope was adopted to observe the pathological morphology of abdominal aorta in mice. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) levels were determined using the ELISA method, whereas Western blotting was used to determine nuclear factor- (NF-) κB p65. Of note, intragastric CQD administration ameliorated ApoE-model mice, as evidenced by reduced levels of FBG, FINS, IRI, TG, TC, and LDL-C. Furthermore, CQD alleviated vascular endothelial injury and regularized the structure of the abdominal aorta by downregulating the expressions of proinflammatory cytokines TNF-α, IL-6, ICAM-1, VCAM-1, and NF-κB p65. Overall, these findings advocated that CQD ameliorates metabolic levels and vascular endothelial injury in mice by downregulating the inflammatory response and thus may be utilized as a novel MetS therapy.
Highlights
Metabolic syndrome (MetS) is a cluster of metabolic diseases that transpire together
Chromatographic separation was carried on a Symmety C18 column and the column temperature was maintained at 25°C. e mobile phase was composed of 0.1% formic acid (A) and acetonitrile (B) with gradient elution system (0–30 min, 90%A; 30–60 min, 90%⟶70%A; 60–100 min, 70%⟶40%A; 100–120 min, 40%⟶10%A) at a flow rate of 0.2 mL/min, and the injection volume was 10 μL. e electrospray ion source (ESI) was used for full scan in both positive and negative modes, 50 psi of nebulizer pressure, 10 L/min of spray gas flow, 350°C of spray gas temperature, 1.00 V of crushing voltage, and 50–1000 m/z of scanning range
Regulatory Effect of ChaiQi decoction (CQD) on Blood Glucose and Insulin in Mice. e fasting blood glucose (FBG) level in the model group was significantly higher compared to the blank control group (P < 0.05), whereas the level in the CQD group was remarkably lower than that in the model group (P < 0.05) (Figure 3(a))
Summary
Metabolic syndrome (MetS) is a cluster of metabolic diseases that transpire together. Is elevates the incidence of MetS which is estimated to be 25% in the United States, 23% in Europe, and 20–25% in South Asia [1]. Research showed that the risk of cardiovascular disease potentially is advanced by the symptoms of MetS and could become severe when several abnormalities occur concomitantly; this causes major adverse cardiac events (MACE) [2]. The probability of cardiovascular diseases and stroke in MetS patients was previously reported to be 2-3 times higher than in nonMetS patients [3]. A prospective analysis conducted to determine the atherosclerosis risk in a community study indicated an 18% greater risk of incident MetS for individuals with the highest western dietary pattern score [4]. MetS symptoms, such as central obesity, dyslipidemia, insulin resistance (IR), and hypertension, are closely associated with vascular endothelial injury, increased intercellular cell adhesion molecule-1(ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1); this promotes inflammation
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