Molecular biology reports · 2023
Metformin-chlorogenic acid combination reduces skeletal muscle inflammation in c57BL/6 mice on high-fat diets.
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Khalafani Zahra, Zamani-Garmsiri Fahimeh, Panahi Ghodratollah, Meshkani Reza
Аннотация
BACKGROUND: Inflammation at the low-grade level has been found to contribute to obesity-induced insulin resistance in the skeletal muscle (SM). This study investigated the anti-inflammatory potential of metformin (MET) combined with chlorogenic acid (CGA) in SM of mice fed a high-fat diet (HFD).
MATERIALS AND METHODS: The C57BL/6 mice were divided into five groups of ten each, normal diet, HFD, HFD + MET, HFD + CGA and HFD + MET + CGA.
RESULTS: The results revealed that MET and CGA, alone or in combination, have a reducing effect on weight gain, plasma triglyceride, glucose and insulin levels. MET in combination with CGA led to attenuation of SM inflammation, an effect that was associated with decreasing macrophages infiltration rate. Combined treatment of MET and CGA also resulted in switching macrophages from M1 to M2 phenotype, presented by the higher expression levels of arginase and CD206 (M2 markers) and lower expression levels of iNOS and cd11c markers (M1). In addition, combination treatment was more effective in increasing the anti-inflammatory cytokines expression (IL-10) and decreasing the expression of pro-inflammatory mediators (TNF-α, IL-1β, MCP-1 and IL-6).
CONCLUSION: These findings suggest that the combination treatment of MET and CGA is likely to be a promising approach to control SM inflammation in the HFD-fed model.
MATERIALS AND METHODS: The C57BL/6 mice were divided into five groups of ten each, normal diet, HFD, HFD + MET, HFD + CGA and HFD + MET + CGA.
RESULTS: The results revealed that MET and CGA, alone or in combination, have a reducing effect on weight gain, plasma triglyceride, glucose and insulin levels. MET in combination with CGA led to attenuation of SM inflammation, an effect that was associated with decreasing macrophages infiltration rate. Combined treatment of MET and CGA also resulted in switching macrophages from M1 to M2 phenotype, presented by the higher expression levels of arginase and CD206 (M2 markers) and lower expression levels of iNOS and cd11c markers (M1). In addition, combination treatment was more effective in increasing the anti-inflammatory cytokines expression (IL-10) and decreasing the expression of pro-inflammatory mediators (TNF-α, IL-1β, MCP-1 and IL-6).
CONCLUSION: These findings suggest that the combination treatment of MET and CGA is likely to be a promising approach to control SM inflammation in the HFD-fed model.