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Effects | Experimental model | Mechanism of action |
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Antioxidative effects | Type 2 diabetic rats | Reduced oxidative stress [62] |
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Hypolipidemic effects | Wistar rats | Decreased blood FFA level and enhanced the activity of lipoprotein lipase [63] |
Type 2 diabetic rats | Increased PPARs and P-TEFb mRNA and protein expression in the adipose tissue. Restored SOD and LPL activity and normalized malondialdehyde, FFA, TNF-α, and adiponectin levels [64] |
3T3-L1 adipocytes | Increased glucose transport and consumption in 3T3-L1 adipocytes [65] |
3T3-L1 adipocytes | Modulated metabolism-related PPARs expression and differentiation-related P-TEFb expression in adipocytes [66] |
3T3-L2 adipocytes | Activated adenosine monophosphate, activated protein kinase [67] |
Diabetic hyperlipidemic and normal rats | Modulated metabolism-related PPAR alpha/delta/gamma protein expression in the liver [68] |
|
Anti-inflammatory actions | Type 2 diabetic rats | Regulated serum levels of inflammatory factors such as CRP, IL-6, TNF-α, and adiponectin [69] |
|
Effects on renal injury | Glomerular mesangial cells | Inhibited NF-κB activation and the expression of its downstream inflammatory factors to improve ECM accumulation and alleviate inflammatory injury in diabetic kidney [70] |
|
Prevention of diabetes complications | Type 2 diabetic rats | Enhanced vascular smooth muscle activity [71] |
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Renal protective effects | Rat glomerular mesangial cells | Reduced the accumulation of extracellular matrix components including fibronectin and prevented the activation of the p38 MAPK signaling pathway [72] |
Diabetic rats | Inhibited glycosylation and exhibited antioxidative effects [73] |
Diabetic C57BL/6 mice | Deactivated the SphK-S1P signaling pathway [74] |
Streptozotocin-induced diabetic rats | Reduced oxidative stress and deactivated aldose reductase [75, 76] |
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