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Background: Ice plant (Mesembryanthemum crystallinum) is a vegetable with various therapeutic uses, one of which is its ability to prevent diabetes. The present study examined the insulin secretion effect related to the mechanism of action of ice plant extract (IPE) and its active compound D-pinitol in a rat insulin-secreting β-cell line, INS-1, as well as in diabetic rats. Methods: The glucose-stimulated insulin secretion (GSIS) test and Western blotting were used to measure GSIS. The glucose-stimulated index (GSI) and expression levels of insulin-related pathway factors, including insulin receptor substrate-2 (IRS-2), phosphoinositide 3-kinase (PI3K), Akt, and pancreatic and duodenal homeobox-1 (PDX-1), were measured in INS-1 cells. Results: The results showed that the GSI values were found to be 8.17 ± 0.22 and 12.21 ± 0.22 for IPE (25 μg/mL) and D-pinitol (100 μM), respectively. GSI values increased statistically significantly. In addition, IPE and D-pinitol upregulated the expression of insulin-related pathway factors. These findings indicate that insulin secretion was significantly stimulated by IPE and D-pinitol in the INS-1 cells, partly by upregulating the expression of IRS-2, PI3K, Akt, and PDX-1. Additionally, IPE administration significantly reduced excessive weight gain and improved glucose tolerance by decreasing the OGTT-AUC. It demonstrated liver-function-improving and lipid-lowering effects by reducing serum alanine aminotransferase (ALT), serum aspartate aminotransferase (AST), triglyceride levels, and total cholesterol levels. Mechanistically, IPE enhances insulin signaling by increasing insulin receptor substrate 1 (IRS-1) phosphorylation and improving glucose metabolism and insulin sensitivity. Conclusions: These results offer important new information on the potential of D-pinitol and IPE as functional foods for improving insulin secretion and managing metabolic dysregulation associated with diabetes. [ABSTRACT FROM AUTHOR]

Macelignan, from Myristica fragrans (nutmeg), is a bioactive compound with various pharmacological properties, including anti-inflammatory and neuroprotective activities. The purpose of this work was to investigate the antioxidant and anti-apoptotic effects of macelignan in glutamate-treated HT22 mouse hippocampal neurons. Macelignan was extracted and identified in a methanol extract of M. fragrans seeds. The DPPH was used to assess the antioxidative activity of macelignan. Glutamate (5 mM) was used to induce neurotoxicity in the HT22 cells. Neuroprotective effects were measured using relevant biochemical and imaging assays, including cell viability, ROS production, nuclear staining, apoptotic cell death, and protein expression. Macelignan markedly and concentration-dependently enhanced DPPH radical scavenging activity. In the HT22 cell model, glutamate induced cell damage by decreasing cell viability, promoting ROS generation, and increasing apoptotic cell death according to cell morphological changes. However, macelignan treatment restored cell viability, inhibited ROS generation concentration-dependently, and reduced apoptosis. Moreover, glutamate significantly up-regulated the phosphorylation of MAPK-pathway-related proteins, which was reversed by macelignan treatment. In conclusion, macelignan shows notable neuroprotective effects on oxidative stress and apoptotic cell death in glutamate-induced cells, and this study provides useful information on its potential therapeutic implications in neurological disorders. [ABSTRACT FROM AUTHOR]

Background: Natural products are gaining attention for their potential benefits in gastrointestinal health. Plant-derived polysaccharides are essential for boosting intestinal immunity and maintaining gut homeostasis. This study investigated the effects of Korean red ginseng polysaccharides (KRG-P) on intestinal homeostasis including IgA and SCFA production and mucosal barrier integrity. Methods: Mice were orally administered KRG-P at doses of 50 mg/kg or 200 mg/kg for 10 days. Fecal IgA levels were measured on days 3, 5, and 11 and IgA from cultured Peyer's patch cells from KRG-P-treated mice were analyzed. Additionally, mRNA and protein expression levels of α-defensin, lysozyme, and E-cadherin in the small intestine were examined. Short-chain fatty acids (SCFAs) content in the cecum was also assessed. Results: KRG-P-treated groups showed a significant increase in fecal IgA levels on days 5 and 11, with no notable change on day 3. Cultured Peyer's patch cells from mice demonstrated heightened IgA production. Additionally, KRG-P administration upregulated α-defensin and lysozyme mRNA expression, along with elevated protein expression of E-cadherin, α-defensin, and lysozyme, in the small intestine. KRG-P treatment also led to increased cecal SCFA levels, including acetate, butyrate, and propionate. Conclusions: KRG-P may promote intestinal homeostasis and host defense mechanisms by activating immune cells in Peyer's patches, stimulating IgA production, enhancing antimicrobial peptide expression, and modulating gut microbiota metabolism through increased SCFA production. [ABSTRACT FROM AUTHOR]

The protective effects of an extract from bitter melon (. Momordica charantia, Cucurbitaceae) against oxidative stress was previously reported and found that protocatechuic acid (PCA) was one of the major phenolic constituents in the extract. The renoprotective effect of PCA from bitter melon was investigated in the present study. In the LLC-PK1 cellular model, the decline in cells viabilities induced by oxidative stress, such as that induced by sodium nitroprusside, pyrogallol, and SIN-1, was significantly and dose-dependently inhibited by PCA. In the in vivo model, the cisplatin-treated rats showed increased plasma levels of creatinine, decreased creatinine clearance, and increased urine protein levels. However, these parameters related to renal dysfunction were markedly attenuated by PCA treatment. Administration of PCA resulted in remarkable improvement in the histological appearance and reduction in tubular cell damage in the cisplatin-treated rat kidneys. Moreover, the elevated levels of pro-caspase-3 induced by cisplatin in rat kidneys were down-regulated by PCA co-treatment. These results suggest that PCA has protective activity against anticancer drug-induced oxidative nephrotoxicity.