Effect of cinnamtannin B‐1 on cholecystokinin‐8‐evoked responses in mouse pancreatic acinar cells

Rivera-Barreno, Ramón; Castillo-Vaquero, Angel del; Salido, Ginés M.; Gonzalez, Antonio

doi:10.1111/j.1440-1681.2010.05424.x

Cited by 21 publications

(5 citation statements)

References 57 publications

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“…By contrast, cpd5 was toxic to INS-1 cells, whereas cpd1 and cpd2 had no protective effect on pancreatic β-cells. The trimer procyanidins, cinnamtannin B1 and D1, inhibit cyclooxygenase-2 [23] , whereas cinnamtannin B1 exerts anti-oxidative effects in pancreatic acinar cells [24] . Our recent study also showed that cinnamtannin D1 protects against PA-induced β-cell dysfunction by attenuating oxidative stress and reducing nuclear factor kappa B (NF-κB) activation [16] .…”

Section: Discussionmentioning

confidence: 99%

Trimer procyanidin oligomers contribute to the protective effects of cinnamon extracts on pancreatic β-cells in vitro

et al. 2016

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Aim: Cinnamon extracts rich in procyanidin oligomers have shown to improve pancreatic β-cell function in diabetic db/db mice. The aim of this study was to identify the active compounds in extracts from two species of cinnamon responsible for the pancreatic β-cell protection in vitro. Methods: Cinnamon extracts were prepared from Cinnamomum tamala (CT-E) and Cinnamomum cassia (CC-E). Six compounds procyanidin B2 (cpd1), (-)-epicatechin (cpd2), cinnamtannin B1 (cpd3), procyanidin C1 (cpd4), parameritannin A1 (cpd5) and cinnamtannin D1 (cpd6) were isolated from the extracts. INS-1 pancreatic β-cells were exposed to palmitic acid (PA) or H 2 O 2 to induce lipotoxicity and oxidative stress. Cell viability and apoptosis as well as ROS levels were assessed. Glucose-stimulated insulin secretion was examined in PA-treated β-cells and murine islets. Results: CT-E, CC-E as well as the compounds, except cpd5, did not cause cytotoxicity in the β-cells up to the maximum dosage using in this experiment. CT-E and CC-E (12.5-50 μg/mL) dose-dependently increased cell viability in both PA-and H 2 O 2 -treated β-cells, and decreased ROS accumulation in H 2 O 2 -treated β-cells. CT-E caused more prominent β-cell protection than CC-E. Furthermore, CT-E (25 and 50 μg/mL) dose-dependently increased glucose-stimulated insulin secretion in PA-treated β-cells and murine islets, but CC-E had little effect. Among the 6 compounds, trimer procyanidins cpd3, cpd4 and cpd6 (12.5-50 μmol/L) dose-dependently increased the cell viability and decreased ROS accumulation in H 2 O 2 -treated β-cells. The trimer procyanidins also increased glucose-stimulated insulin secretion in PA-treated β-cells. Conclusion: Trimer procyanidins in the cinnamon extracts contribute to the pancreatic β-cell protection, thus to the anti-diabetic activity.

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Section: Discussionmentioning

confidence: 99%

Trimer procyanidin oligomers contribute to the protective effects of cinnamon extracts on pancreatic β-cells in vitro

et al. 2016

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“…17 As reported, the main components of extracts were A-type procyanidin trioligomers, including >43% CD1 and >23% CB1, one structural isomer of CD1. 17 A-type polymers were reported to reduce peroxide-induced pancreatic acinar cell injury, 27,28 generate insulin-like biological activity, 13 and improve insulin sensitivity in vivo. 29 However, as effective antioxidants 24 and the major components of antidiabetic natural products, 17 the effects of A-type polymers in C. tamala have not yet been explored on insulin-secreting β-cells.…”

Section: ■ Discussionmentioning

confidence: 99%

Cinnamtannin D-1 Protects Pancreatic β-Cells from Palmitic Acid-Induced Apoptosis by Attenuating Oxidative Stress

Wang

Sun

Chen

et al. 2014

J. Agric. Food Chem.

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In previous studies, A-type procyanidin oligomers isolated from Cinnamomum tamala were proved to possess antidiabetic effect and protect pancreatic β-cells in vivo. The aim of this study was to unveil the mechanisms of protecting pancreatic β-cells from palmitic acid-induced apoptosis by cinnamtannin D-1 (CD1), one of the main A-type procyanidin oligomers in C. tamala. CD1 was discovered to dose-dependently reduce palmitic acid- or H2O2-induced apoptosis and oxidative stress in INS-1 cells, MIN6 cells, and primary cultured murine islets. Moreover, CD1 could reverse palmitic acid-induced dysfunction of glucose-stimulated insulin secretion in primary cultured islets. These results indicate that reduction of apoptosis and oxidative stress might account for the protection effect of CD1, which provided a better understanding of the mechanisms of the antidiabetic effects of procyanidin oligomers.

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“…This could represent a pathogenetic mechanism of autodigestion of the gland that might lead to the onset of pancreatic inflammation [68]. The underlying cause responsible for the impairment of enzyme secretion could involve intracellular Ca 2+ accumulation and concomitant oxidative stress [69][70][71]. The relationship between AA and Ca 2+ signaling has been studied (see above).…”

Section: Role Of Arachidonic Acid In Pancreatitis and Diabetesmentioning

confidence: 99%

Membrane Lipid Derivatives: Roles of Arachidonic Acid and Its Metabolites in Pancreatic Physiology and Pathophysiology

et al. 2023

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One of the most important constituents of the cell membrane is arachidonic acid. Lipids forming part of the cellular membrane can be metabolized in a variety of cellular types of the body by a family of enzymes termed phospholipases: phospholipase A2, phospholipase C and phospholipase D. Phospholipase A2 is considered the most important enzyme type for the release of arachidonic acid. The latter is subsequently subjected to metabolization via different enzymes. Three enzymatic pathways, involving the enzymes cyclooxygenase, lipoxygenase and cytochrome P450, transform the lipid derivative into several bioactive compounds. Arachidonic acid itself plays a role as an intracellular signaling molecule. Additionally, its derivatives play critical roles in cell physiology and, moreover, are involved in the development of disease. Its metabolites comprise, predominantly, prostaglandins, thromboxanes, leukotrienes and hydroxyeicosatetraenoic acids. Their involvement in cellular responses leading to inflammation and/or cancer development is subject to intense study. This manuscript reviews the findings on the involvement of the membrane lipid derivative arachidonic acid and its metabolites in the development of pancreatitis, diabetes and/or pancreatic cancer.

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Effect of cinnamtannin B‐1 on cholecystokinin‐8‐evoked responses in mouse pancreatic acinar cells

Cited by 21 publications

References 57 publications

Trimer procyanidin oligomers contribute to the protective effects of cinnamon extracts on pancreatic β-cells in vitro

Trimer procyanidin oligomers contribute to the protective effects of cinnamon extracts on pancreatic β-cells in vitro

Cinnamtannin D-1 Protects Pancreatic β-Cells from Palmitic Acid-Induced Apoptosis by Attenuating Oxidative Stress

Membrane Lipid Derivatives: Roles of Arachidonic Acid and Its Metabolites in Pancreatic Physiology and Pathophysiology

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