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Crocin prevents metabolic syndrome in rats via enhancing PPAR-gamma and AMPK.

ABSTRACT: Metabolic syndrome (Mets) is a major health hazard. The syndrome is strongly linked to cardiovascular disease. The objective of the current study was to address whether or not crocin could protect against experimentally-induced MetS in rats as well as the possible underlying mechanisms. Animals were allocated into 4 groups. The first one served as control and was kept on regular food pellets and drinking water. The other three groups were subjected to experimental MetS. Induction of MetS was achieved by keeping rats on food pellets containing 3% NaCl; and drinking water enriched with 10% fructose. The first and second groups were daily gavaged with saline. The third and fourth groups were daily administered crocin 5 and 10 mg/kg, respectively. The treatment continued for 12 consecutive weeks. Crocin significantly reduced body weight gain and adiposity index as compared to MetS group. Also, crocin protected against the occurrence of hyperglycemia and insulin resistance as indicated by controlled values of HOMA-IR. Crocin protected against MetS-induced dyslipidemia as well as the rise blood pressure. These beneficial effects were accompanied by enhanced serum levels of PPAR? & AMPK and inhibited serum levels of IL-6 and TNF-?. In conclusion, crocin protects against experimentally-induced MetS. This can be attributed, at least partly, to activation of PPAR? and AMPK as well as inhibiting inflammation.

SUBMITTER: Algandaby MM

PROVIDER: S-EPMC7182989 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

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Crocin prevents metabolic syndrome in rats via enhancing PPAR-gamma and AMPK.

Algandaby Mardi M MM

Saudi journal of biological sciences 20200127 5

Metabolic syndrome (Mets) is a major health hazard. The syndrome is strongly linked to cardiovascular disease<b>.</b> The objective of the current study was to address whether or not crocin could protect against experimentally-induced MetS in rats as well as the possible underlying mechanisms. Animals were allocated into 4 groups. The first one served as control and was kept on regular food pellets and drinking water. The other three groups were subjected to experimental MetS. Induction of MetS ...[more]

PMID: 32346340

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Project description:Transient receptor potential channel C6 (TRPC6) gain-of-function mutations and increased TRPC6 expression in podocytes induce glomerular injury and proteinuria. Sildenafil reduces TRPC6 expression and activity in nonrenal cell types, although the mechanism is unknown. Peroxisome proliferator-activated receptor γ (PPAR-γ) is a downstream target of sildenafil in the cyclic guanosine monophosphate (cGMP)-activated protein kinase G (PKG) axis. PPAR-γ agonists, like pioglitazone, appear antiproteinuric. We hypothesized that sildenafil inhibits TRPC6 expression in podocytes through PPAR-γ-dependent mechanisms, thereby counteracting podocyte injury and proteinuria. Treatment with sildenafil, the cGMP derivative 8-bromoguanosine 3',5'-cyclic monophosphate sodium salt (8-Br-cGMP), or pioglitazone dose-dependently downregulated podocyte injury-induced TRPC6 expression in vitro Knockdown or application of antagonists of PKG or PPAR-γ enhanced TRPC6 expression in podocytes and counteracted effects of sildenafil and 8-Br-cGMP. We observed similar effects on TRPC6 promoter activity and TRPC6-dependent calcium influx. Chromatin immunoprecipitation showed PPAR-γ binding to the TRPC6 promoter. Sildenafil or pioglitazone treatment prevented proteinuria and the increased TRPC6 expression in rats with adriamycin-induced nephropathy and mice with hyperglycemia-induced renal injury. Rats receiving PPAR-γ antagonists displayed proteinuria and increased podocyte TRPC6 expression, as did podocyte-specific PPAR-γ knockout mice, which were more sensitive to adriamycin and not protected by sildenafil. Thus, sildenafil ameliorates podocyte injury and prevents proteinuria through cGMP- and PKG-dependent binding of PPAR-γ to the TRPC6 promoter, which inhibits TRPC6 promoter activity, expression, and activity. Because sildenafil is approved for clinical use, our results suggest that additional clinical study of its antiproteinuric effect in glomerular disease is warranted.

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Crocin prevents metabolic syndrome in rats via enhancing PPAR-gamma and AMPK.

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Crocin prevents metabolic syndrome in rats via enhancing PPAR-gamma and AMPK.

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