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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]

Senescence can promote hyperplastic pathologies, such as cancer. Prostate cancer is the second most common type of cancer in men. The p21-mediate cellular senescence, facilitated through the tumor suppressor p53-dependent pathway, is considered the primary mechanism for cancer treatment. Aloe-emodin, has been reported to exert anticancer effects in various types of cancers. This study aimed to investigate the bioactivity of aloe-emodin in LNCaP cells via the activation of p21-mediated cellular senescence. Aloe-emodin treatment increased the percentage of cells in the G1 phase while decreasing the percentage in the S phase. This effect was reflected in the expression levels of proteins associated with cell cycle progression, such as p21CIP, retinoblastoma protein, and cyclin-dependent kinase2/4 in LNCaP cells. However, aloe-emodin-treated LNCaP cells did not induce cell cycle arrest at G2/M checkpoint. Moreover, increased senescence-associated-galactosidase activity was observed in a dose-dependent manner following treatment with aloe-emodin. Aloe-emodin also induced DNA damage by modulating the expression of histone H2AX and lamin B1. Furthermore, aloe-emodin inhibited the proliferation of LNCaP cells, contrasting with the exponential growth observed in the nontreated cells. Importantly, this inhibition did not impact the immune system, as evidenced by the increased proliferation of splenocytes isolated from mice. These findings provide preliminary evidence of the anticancer effect of aloe-emodin in LNCaP cells, necessitating further investigations into the underlying mechanisms in vivo and human subjects. [ABSTRACT FROM AUTHOR]

So Shiho Tang (SSHT) is a traditional herbal medicine commonly used in Asian countries. This study evaluated the anti-inflammatory effect of SSHT and the associated mechanism using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and murine dextran sodium sulfate (DSS)-induced ulcerative colitis models. Pre-treatment of RAW 264.7 macrophages with SSHT significantly reduced LPS-induced inflammation by decreasing nitrite production and regulating the mitogen-activated protein kinase pathway. Meanwhile, in mice, DSS-induced colitis symptoms, including colon shortening and body weight loss, were attenuated by SSHT. Moreover, representative compounds of SSHT, including glycyrrhizic acid, ginsenoside Rb1, baicalin, saikosaponin A, and saikosaponin B2, were quantified, and their effects on nitrite production were measured. A potential anti-inflammatory effect was detected in LPS-induced RAW 264.7 cells. Our findings suggest that SSHT is a promising anti-inflammatory agent. Its representative components, including saikosaponin B2, ginsenoside Rb1, and baicalin, may represent the key active compounds responsible for eliciting the anti-inflammatory effects and can, therefore, serve as quality control markers in SSHT preparations. [ABSTRACT FROM AUTHOR]

The present study investigated potential bioactive natural products from the EtOH extract of Salix chaenomeloides twigs using column chromatography, leading to the isolation of six compounds (1–6), which were characterized as two proanthocyanidins, procyanidin B2 (1) and procyanidin B1 (2), and four phenolic compounds, 4-hydroxybenzoic acid β-D-glucosyl ester (3), di-O-methylcrenatin (4), p-coumaric acid glucoside (5), and syringin (6) by the comparison of their NMR spectra with the reported data and high-resolution (HR)-electrospray ionization mass spectroscopy (ESI-MS) analysis. We investigated the potential of six compounds (1–6) to inhibit adipogenesis in 3T3-L1 preadipocytes, which showed that the compounds (1–6) significantly reduced lipid accumulation in 3T3-L1 adipocytes without affecting cell proliferation. Notably, compound 1 demonstrated a remarkable 60% and 90% reduction in lipid levels with 50 and 100 µM treatments, respectively. Oil Red O staining results indicated that compound 1 significantly inhibits the formation of lipid droplets, comparable to the effect of T863, an inhibitor of triglyceride used as a positive control, in adipocytes. Compound 1 had no effect on the regulators PPARγ, C/EBPα, and SREBF1 of adipocyte differentiation in 3T3-L1 preadipocytes, but compound 1 activated the fatty acid oxidation regulator, PPARα, compared to the lipogenic-induced control. It also suppressed fatty acid synthesis by downregulating the expression of fatty acid synthase (FAS). Finally, compound 1 induced the mRNA and protein levels of CPT1A, an initial marker of mitochondrial fatty acid oxidation in 3T3-L1. This finding substantiates the anti-lipogenic and lipolytic effects of procyanidin B2 (1) in 3T3-L1 preadipocytes, emphasizing its pivotal role in modulating obesity-related markers. [ABSTRACT FROM AUTHOR]