13th Congress of the Asian Society of Transplantation: General transplantation issueExperimental transplantationGinsenoside Rg3 Enhances Islet Cell Function and Attenuates Apoptosis in Mouse Islets
Section snippets
Animals
Female Balb/c mice (12 weeks of age) were purchased from Jeung-Do Bio Plant Co (Seoul, Korea). Our study was reviewed and approved by the Animal Care and Use Committee of Korea Institute of Science and Technology (Gangneung, Korea).
20(S)-Ginsenoside Rg3 (Rg3)
Rg3 was purchased from Ambo Institute (South Korea), and dissolved in 0.1% dimethyl sulfoxide (DMSO). The chemical structure of Rg3 is shown in Fig 1.
Mouse Islet Isolation
Islets were isolated from Balb/c mice pancreas by a collagenase digestion procedure. After isolation, islets were
Results
Islet cell viability was assessed by diacetate–propidium iodide staining at 24, 48, and 72 hours after the isolation procedure. Viability values for the Rg3 groups were similar to those of the control groups at 24, 48, and 72 hours and showed no statistical difference between the 2 groups (Fig 2A). Rg3 suppressed the cleavage of PARP. PARP (116 kDa) is cleaved to produce an 89-kDa fragment during apoptosis. PARP cleavage, as evidenced by the accumulation of the 89-kDa species, was observed when
Discussion
This study indicates that mouse islet function (glucose-stimulated insulin secretion) can be increased by simple Rg3 culturing methods after the isolation procedure. In addition, we observed lower apoptotic levels in islets isolated from Rg3-cultured groups, indicating less inflammatory damage.
Islet transplantation is a promising treatment of diabetes mellitus [1]. However, it faces several challenges, including the loss of islet cell viability and function during the peritransplantation
References (9)
- et al.
Islet transplantation in seven patients with type 1 diabetes mellitus using a glucocorticoid-free immunosuppressive regimen
N Engl J Med
(2000) - et al.
Islet cell transplantation: the future?
Langenbecks Arch Surg
(2000) - et al.
Histogenesis and ultrastructure of pancreatic islet graft microvasculature: evidence for graft revascularization by endothelial cells of host origin
Am J Pathol
(1995) - et al.
Heat shock inhibits cytokine-induced nitric oxide synthase expression by rat and human islets
Endocrinology
(1998)
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Herbal remedies, toxicity, and regulations
2020, Preparation of Phytopharmaceuticals for the Management of Disorders: The Development of Nutraceuticals and Traditional MedicineAnti-diabetic properties of different fractions of Korean red ginseng
2019, Journal of EthnopharmacologyCitation Excerpt :We, however, propose that anti-inflammatory properties of KRG may be attributed to NSpn based on our results that KRG and NSpn ameliorated chronic inflammation, as measured by TNF-α, while Spn exhibited no effect in our model. Previous studies demonstrated that KRG (Kim and Kim, 2008) and Rg3 (Kim et al., 2014) enhanced glucose-stimulated insulin secretion in isolated rodent islets. In addition, another form of ginsenoside, Rh2, was also shown to improve insulin secretion through β-cell proliferation in rodents (Lee et al., 2006; Wang et al., 2012).
Protective effect of triterpenes against diabetes-induced β-cell damage: An overview of in vitro and in vivo studies
2018, Pharmacological ResearchCitation Excerpt :Ginsenosides are currently being investigated and have shown superior activity to ameliorative various metabolic complications, including diabetes [148–152]. Using different models, ranging from INS-1 cells, Rin-m5F cells, MIN6 cells, STZ or alloxan-induced diabetic animals, ginsenosides have proved to be beneficial in improving insulin secretion, while suppressing cytokine-induced cell apoptosis [149–161]. Some of the implicated mechanisms include modulation of ERK and p38 MAPK pathways, regulation of protein kinase A (PKA)-dependent pathways, inactivation of FOXO1, and activation of AKT.
Chronic saponin treatment attenuates damage to the pancreas in chronic alcohol-treated diabetic rats
2017, Journal of Ginseng ResearchCitation Excerpt :In the study of Kim et al [8], exposure of 7-wk-old male C57BL/6 mice to ethanol for 8 wk led to a decrease of insulin expression as well as a significant reduction in islet cell mass. It has been reported that saponin induces insulin expression in islets via the protection of islet cells against apoptosis [45,46]. Taken together, chronic saponin exposure in normal and diabetic rats inhibits the decrease in insulin expression induced by ethanol.
Stereoselective pharmacokinetic and metabolism studies of 20(S)- and 20(R)-ginsenoside Rg<inf>3</inf> epimers in rat plasma by liquid chromatography-electrospray ionization mass spectrometry
2016, Journal of Pharmaceutical and Biomedical AnalysisCitation Excerpt :Panax notoginseng possesses dammarane-type tetracyclic triterpenoid ginsenosides as its saponin content exclusively [1]. Among these saponins, ginsenoside Rg3 is a potent compound which executes a wide range of pharmacological effects, including anti-inflammatory [2], antioxidant [3], anti-diabetic [4], and neuroprotective [5] activities, etc. Moreover, ginsenoside Rg3 is proved to be a potent anticancer agent in the treatment of lung [6], breast [7], hepatic [8], pancreatic [9] cancer and melanoma [10] etc.
Effects of ginsenoside Rb1 on hypertrophic scar remodeling in rabbit model
2015, European Journal of PharmacologyCitation Excerpt :As for anti-diabetic effects, ginsenoside Rg3 was efficient in the inhibition of adipocyte differentiation in 3T3-L1 cells through activated AMPK (AMP-activated protein kinase). Ginsenoside Rg3 improved insulin signaling and glucose uptake primarily by stimulating the expression of insulin receptor substrate-1 and glucose transporter type-4 in L6 myotubes, moreover ginsenoside Rg3 enhanced glucose-stimulated insulin secretion in HIT-T15 cells (Kim et al., 2014; Park et al., 2008). Of note, the presumed active constituents of ginseng extracts may be a source of adverse effects and drug interactions.
Funding: Gangneung Asan Hospital Biomedical Research Center Promotion Fund.