Postprandial hyperglycemia and oxidative stress are important factors that worsen the health condition of patients with type 2 diabetes. We recently showed that extracts from Ceiba pentandra mitigate hyperglycemia in dexamethasone‐ and high diet/streptozotocin‐induced diabetes. Herein, we evaluated the postprandial regulatory properties and the antioxidant effects of the aqueous (AE) and methanol (ME) extracts from the stem bark of Ceiba pentandra. The phytochemical analysis of AE and ME was performed using the LC‐MS technique and the total phenolic and flavonoid assays. Both extracts were tested for their ability to inhibit superoxide anion (O₂^•ـ), hydrogen peroxide (H₂O₂), protein oxidation, alpha‐amylase, and alpha‐glucosidase activities. The mode of enzyme inhibition was also determined in a kinetic study. AE and ME were both rich in phenolic and flavonoid compounds. ME was 2.13 and 1.91 times more concentrated than AE in phenolic and flavonoid compounds, respectively. LC‐MS allowed the identification of 5 compounds in both extracts. ME and AE inhibited O₂^•ـ with IC₅₀ of 51.81 and 34.26 μg/ml, respectively. On H₂O₂, they exhibited IC₅₀ of 44.84 and 1.78 μg/ml, respectively. Finally, they exhibited IC₅₀ of 120.60 and 140.40 μg/ml, respectively, in the inhibition of protein oxidation induced by H₂O₂, while showing IC₅₀ of 39.26 and 97.95 μg/ml on the protein oxidation induced by AAPH. ME and AE inhibited alpha‐amylase with IC₅₀ of 6.15 and 54.52 μg/ml, respectively. These extracts also inhibited alpha‐glucosidase, demonstrating IC₅₀ of 76.61 and 86.49 μg/ml. AE exhibited a mixed noncompetitive inhibition on both enzymes, whereas ME exhibited a competitive inhibition on α‐amylase and a pure noncompetitive inhibition on α‐glucosidase. These results demonstrate that ME and AE scavenge reactive oxygen species and prevent their effects on biomolecules. Besides, ME and AE inhibit carbohydrate digestive enzymes. These properties may contribute to reduce postprandial hyperglycemia and regulate glycemia in diabetic patients.

The antidiabetic effects of the methanol extract of the stem bark of Ceiba pentandra (Cp) have been demonstrated in various experimental models. Besides, this extract is rich in 8-formyl-7-hydroxy-5-isopropyl-2-methoxy-3-methyl-1,4-naphthaquinone, 2,4,6-Trimethoxyphenol and vavain. However, it remains unknown whether Cp can mitigate cardiometabolic syndrome (CMS). The present study assessed the curative properties of Cp against Monosodium Glutamate (MSG)-induced CMS in rats. Male neonate Wistar rats were intraperitoneally administered with MSG (4 mg/g/day) during the first 5 days of life (postnatal days 2-6). They were kept under standard breeding conditions up to 5 months of age for the development of CMS. Diseased animals were then orally treated with atorvastatin (80 mg/kg/d) or Cp (75 and 150 mg/kg/day) for 28 days during which food intake, body mass, blood pressure, heart rate, glucose, and insulin tolerance were monitored. Plasma and tissues were collected on day 29th to assess the lipid profile, oxidative stress, and inflammatory parameters. The histomorphology of the adipose tissue was also evaluated. Cp significantly (p < 0.001) reduced the obesogenic and lipid profiles, adipocyte size, blood pressure, and oxidative and inflammatory status in MSG-treated rats. Cp also ameliorated glucose (p < 0.05) and insulin sensitivities (p < 0.001) hence, reducing animals' cardiometabolic risk score (p < 0.001). The curative effect of Cp on cardiometabolic syndrome is related to its capacity to reduce oxidative stress, inflammation, dyslipidemia, and increase insulin sensitivity. These results demonstrate the potential of Cp as a good candidate for alternative treatment of CMS.

Background/Objectives: Toothpaste ingredients such as strontium chloride (SrCl₂) and potassium carbonate (K₂CO₃) are recognized for their desensitizing and remineralizing effects but may be absorbed through the oral mucosa. Their potential cytotoxic and cardiotoxic properties, however, remain inadequately characterized. Here, we investigated the effects of SrCl₂ and K₂CO₃ on mouse-induced pluripotent stem cells (iPSCs) and iPSC-derived cardiomyocytes (iPSC-CMs). Methods: Cells were exposed to varying concentrations of each compound for up to 72 h. Real-time cell analysis (xCELLigence RTCA Cardio system) was used to assess proliferation, and flow cytometry was used to evaluate cell viability. Functional properties of iPSC-CMs were examined using multi-electrode array (MEA) recordings and xCELLigence-based impedance measurements. Cardiac marker expression was examined via immunofluorescence and quantitative RT-PCR. Results: Both SrCl₂ and K₂CO₃ affected iPSC proliferation and reduced viability in a dose- and time-dependent manner, accompanied by altered embryoid body (EB) morphology and increased cell death. In iPSC-CMs, both compounds downregulated key cardiac genes and disrupted spontaneous beating activity, with effects intensifying at higher concentrations. Conclusions: These results demonstrate that SrCl₂ and K₂CO₃ induced dose-dependent cytotoxic and arrhythmogenic effects on iPSCs and iPSC-CMs. At elevated concentrations, these compounds impair iPSC-CM function and may pose safety concerns upon chronic exposure. Further mechanistic and long-term in vivo studies are warranted to assess their potential cardiotoxic risk in consumer oral care products.

Background/Objectives: Toothpaste ingredients such as strontium chloride (SrCl₂) and potassium carbonate (K₂CO₃) are recognized for their desensitizing and remineralizing ef-fects but may be absorbed through the oral mucosa. Their potential cytotoxic and cardio-toxic properties, however, remain inadequately characterized. Here, we investigated the effects of SrCl₂ and K₂CO₃ on mouse-induced pluripotent stem cells (iPSCs) and iPSC-derived cardiomyocytes (iPSC-CMs). Methods: Cells were exposed to varying con-centrations of each compound for up to 72 h. Real-time cell analysis (xCELLigence RTCA Cardio system) was used to assess proliferation, and flow cytometry was used to evaluate cell viability. Functional properties of iPSC-CMs were examined using multi-electrode ar-ray (MEA) recordings and the xCELLigence based impedance measurements. Cardiac marker expression was examined via immunofluorescence and quantitative RT-PCR. Results: Both SrCl₂ and K₂CO₃ affected iPSCs proliferation and reduced viability in a dose- and time-dependent manner, accompanied by altered embryoid body (EB) morphology and increased cell death. In iPSC-CMs, both compounds downregulated keys cardiac genes and disrupted spontaneous beating activity, with effects intensifying at the higher concentrations. Conclusions: These results demonstrate that SrCl₂ and K₂CO₃ induced dose-dependent cytotoxic and arrhythmogenic effects on iPSCs and iPSC-CMs. At elevated concentrations, these compounds impair iPSC-CMs function and may pose safety con-cerns upon chronic exposure. Further mechanistic and long-term in vivo studies are war-ranted to assess their potential cardiotoxic risk in consumer oral care products.

Cardiometabolic diseases are among the main leading causes of morbidity and mortality over the world. The coexistence of a bundle of metabolic risk factors in an individual has prompted Reaven to consider it as a syndrome, called “X syndrome”. The term has later evolved and the health condition is today called “cardiometabolics syndrome” (CMS). Significant progress in the understanding of the pathophysiology of the CMS has been made during the past years. Being able to adequately assess cardiometabolic risk (CMR) is crucial for proper diagnosis, prevention, and better management of CMS, as this could be helpful to slow down its progression and complications. This could also be useful in the preclinical and clinical evaluation of potential treatment strategies. Several methods have been developed to assess the risk of developing cardiometabolic diseases in chronic and clinical setting. However, these methods show limitations when applying to short and experimental settings involving rodents. Therefore, this commentary aims at redefining and highlighting the main risk factors to be reconsidered in cardiometabolic syndrome definition; and proposing a comprehensive estimation method for the evaluation of the CMR in rodents. This is relevant for an appropriate utilization of the term CMS and a deep evaluation of therapeutic targets in experimental settings.