Abstract
Background: Metabolic syndrome (MS) is a global epidemic that has great socioeconomic and public health implications. This study reports observed effects of the Shexiang Baoxin Pill (SBP) in a rat model of MS and explores its underlying mechanisms of action.Methods: A diet-induced rat model of MS was established according to accepted methods, and the rats were randomly divided into two groups: a control group (0.9% NaCl, 100 mg/kg•d) and a SBP-treated group (SBP, 100 mg/kg•d). Systolic blood pressures, fasting blood glucose (FBS) levels, triglyceride (TG) levels, high-density lipoprotein cholesterol (HDL-C) levels, body weights, and abdominal perimeters were dynamically monitored and analyzed. Serum leptin, adiponectin, TNF-α, IL-6, and IL-10 levels were measured by ELISA. Leptin, adiponectin, TNF-α, IL-6, and IL-10 expression in adipose tissue, as well as AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α) expression in heart, liver, skeletal muscle, and adipose tissue was measured by western blot. Expression of the mitochondrial protein UCP2, Cytochrome b and ATPase was observed by immunofluorescent staining.Results: SBP significantly decreased serum TG, TC, LDL-C levels and increased HDL-C levels. SBP also optimized the leptin/adiponectin ratio by decreasing leptin expression and increasing adiponectin expression in adipose tissue. SBP antagonized inflammatory reactions by promoting IL-10 expression in adipose tissue while inhibiting TNF-α and IL-6 expression. SBP improved lipid metabolism by up-regulating the expression of AMPK and PGC-1α. Furthermore, SBP decreased the severity of MS and its complications by adjusting the expression of several mitochondrial proteins, including UCP2, Cytochrome b and ATPase.Conclusion: SBP exhibits prominent therapeutic effects in the setting of MS. Possible mechanisms of action may be related to its anti-inflammatory and anti-oxidative characteristics, as well as its effects on improving lipid metabolism and protecting mitochondrial function.
Highlights
MATERIALS AND METHODSThe incidence of metabolic syndrome (MS) is on the rise globally
A leptin/adiponectin imbalance was found to be associated with increased waist circumference, a diminished vascular response to acetylcholine and greater vasoconstriction in response to angiotensin II (Lopez-Jaramillo, 2016)
Central obesity and disorders of adipose tissue were thought to be the etiologic factors of Metabolic syndrome (MS), with heredity, aging, lack of physical activity and the inflammatory response contributing to the pathogenesis of this condition (Okosun et al, 2000)
Summary
Metabolic syndrome (MS) is a global epidemic that has great socioeconomic and public health implications. This study reports observed effects of the Shexiang Baoxin Pill (SBP) in a rat model of MS and explores its underlying mechanisms of action. Adiponectin, TNF-α, IL-6, and IL-10 expression in adipose tissue, as well as AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α) expression in heart, liver, skeletal muscle, and adipose tissue was measured by western blot. Expression of the mitochondrial protein UCP2, Cytochrome b and ATPase was observed by immunofluorescent staining. SBP improved lipid metabolism by up-regulating the expression of AMPK and PGC-1α. SBP decreased the severity of MS and its complications by adjusting the expression of several mitochondrial proteins, including UCP2, Cytochrome b and ATPase. Possible mechanisms of action may be related to its anti-inflammatory and anti-oxidative characteristics, as well as its effects on improving lipid metabolism and protecting mitochondrial function
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