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Shexiang Baoxin Pill Corrects Metabolic Disorders in a Rat Model of Metabolic Syndrome by Targeting Mitochondria

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 w...

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Detalles Bibliográficos
Autores principales: Wei, Dan, Zheng, Ningning, Zheng, Lanyan, Wang, Leting, Song, Liang, Sun, Luning
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841394/
https://www.ncbi.nlm.nih.gov/pubmed/29551973
http://dx.doi.org/10.3389/fphar.2018.00137
Descripción
Sumario: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.