| Objective To explore the effects of mangiferin on the renal interstitial fiber deposition induced by high fructose consumption in spontaneously hypertensive rats (SHRs).Methods 24 SHRs were randomly divided into 4 groups:control group, fructose group, fructose+mangiferin (5 mg/kg) and fructose+mangiferin (15 mg/kg) groups. After 7 week feeding, rats were sacrificed, blood samples were collected for determination of plasma concentrations of glucose, triglyceride, total cholesterol and non-esterified fatty acid. The indexes of lipid in kidney were determined histologically and enzymatically. The renal interstitial fiber deposition were observed by Masson staining. The renal expression of MCP-1, CD68, a-SMA, co14a4, TGF-?, PAI-1 and uPA mRNA were detected by Real time PCR. And the protein expression of uPA and PAI-1 was examined by immunohistochemistry.Results Mangiferin (15 mg/kg) could significantly reduce SHR renal interstitial fiber deposition induced by fructose consumption. There is no marked change in renal triglycerides content among groups, the mRNA expression of MCP-1, CD68, a-SMA, col4a4, TGF-? in kidneys also no change, but mangiferin (15 mg/kg) apparently reversed the uPA/PAI-1 mRNA ratio reduced by fructose consumption, decreased the overexpression of PAI-1 protein induced by fructose consumption.Conclusion Mangiferin could improve renal interstitial fiber deposition induced by high fructose consumption in SHRs, which may be related to modulation of renal PAI-1 and uPA.Objective:To explore the effects of mangiferin on the insulin resistance induced by high fructose consumption in rats.Method:18 Wistar-Kyoto rats (WKY) and 18 spontaneously hypertensive rats (SHRs) were divided into 6 groups (n=6 per group):(1) WKY control,free access to water; (2) WKY fructose control, free access to 10% fructose solution; (3) WKY fructose+mangiferin (15mg/kg); (4) SHR control, free access to water; (5) SHR fructose control, free access to 10% fructose solution; (6) SHR fructose+mangiferin (15mg/kg). At the end of week 6, oral glucose tolerance test (OGTT) was performed. Plasma concentrations of glucose, insulin, triglyceride and NEFA were determined. Adipo-IR index was calculated as the following formula:[Adipo-IR index = fasted insulin (mmol/L) x fasted NEFA (pmol/L)], while the hepatic insulin sensitivity was expressed as the homeostasis model assessment of insulin resistance (HOMA-IR) index{[fasted insulin (?IU/mL) x fasted glucose (mM)]/22.5). Plasma TG and NEFA clearance were counted and analysed. Animals were euthanized after being fasted overnight at the end of week 7. The geen expression of CD36 was determined by Real time PCR, and the protein expression was showed by Western blot and immunofluorescence staining.Result:High-fructose feeding induced increases in plasma insulin concentrations at baseline and during oral glucose tolerance test (OGTT), the homeostasis model assessment of insulin resistance (HOMA-IR) index, and the adipose tissue insulin resistance index in WKY. Furthermore, fructose feeding increased the clearance of plasma non-esterified fatty acid (NEFA) during OGTT. These adverse effects were attenuated in SHR. Co-administration of mangiferin mitigated the fructose-induced hyperinsulinemia/insulin resistance and increase in the clearance of plasma NEFA during OGTT in WKY. However, it showed minimal effect on insulin concentrations and plasma NEFA clearance during OGTT in fructose-fed SHR. By Real time PCR and Western blot, we found that there was not significantly difference in total muscular expression of CD36 mRNA and protein in WKY. Immunofluorescence staining revealed that mangiferin treatment suppressed fructose-stimulated sarcolemma overexpression of CD36 in the gastrocnemius of WKY.Conclusion:Mangiferin treatment mitigates fructose-induced insulin resistance in rats may via a CD36-related pathway. |
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