Cytoprotective Effects of KIOM-79 on Streptozotocin Induced Cell Damage by Inhibiting ERK and AP-1

Kang, Kyoung Ah; Lee, Kyoung Hwa; Kim, So Young; Kim, Hee Sun; Kim, Jin Sook; Hyun, Jin Won

doi:10.1248/bpb.30.852

Cited by 24 publications

(21 citation statements)

References 39 publications

(26 reference statements)

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“…Since, oxidative stress induced cell death is caused by increased NO generation, altered mitochondrial membrane potential and/or activation of caspases, interference with these events has been suggested to protect pancreatic β-cells from oxidative stress induced apoptosis [62]. Our results suggest that GLEt contains chemical substances which could possibly interfere with these events and thus able to protect β-cells from alloxaninduced apoptosis.…”

Section: Discussionmentioning

confidence: 67%

Gymnema montanum H. Protects Against Alloxan-induced Oxidative Stress and Apoptosis in Pancreatic β-cells

Ramkumar

Lee²,

Krishnamurthi³

et al. 2009

Cell Physiol Biochem

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The present study evaluated the molecular mechanism of antidiabetic property of G. montanum leaf extract (GLEt) against alloxan-induced apoptotic cell death in rat insulinoma cells (RINm5F). The pre-treatment of GLEt (5 μg and 10 μg/ml) resulted in significant decrease in intracellular Ca²⁺ concentration, nitric oxide (NO) production along with increase in mitochondrial membrane potential in alloxan (7mM/ml) treated cells. Further GLEt reduced apoptosis by inhibiting the release of cytochrome c and subsequent cleavage of PARP and caspase-3. The immunochemical staining of 8-hydroxydeoxyguanosine (8-OHdG) also evidenced the suppression of oxidative stress by GLEt. The cell cycle analysis, annexin-V labelling assay and TUNEL assay showed the suppression of apoptosis by the treatment of GLEt. Moreover, GLEt significantly increased the cellular antioxidant levels and decreased the lipid peroxides in alloxan-treated RINm5F cells. Taken together, these findings suggest that G. montanum protects pancreatic β-cells against reactive oxygen species (ROS) by counteracting with mitochondrial membrane permeability and inhibition of the apoptotic pathway.

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Section: Discussionmentioning

confidence: 67%

Gymnema montanum H. Protects Against Alloxan-induced Oxidative Stress and Apoptosis in Pancreatic β-cells

Ramkumar

Lee²,

Krishnamurthi³

et al. 2009

Cell Physiol Biochem

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“…KIOM-79 has anti-inflammatory [16], anti-diabetic, anti-hyperglycemic and anti-retinal damage effects [14][15][16][17][18][19]. KIOM-79 cytoprotects pancreatic β-cells by inhibiting streptozotocin (STZ)-induced oxidative stress [20][21][22]. In the present study, the cytoprotective mechanisms of KIOM-79 were identified in the ER stress-mediated apoptosis pathway by STZ in pancreatic β-cells.…”

Section: Introductionmentioning

confidence: 66%

“…In our previous study, reactive oxygen species scavenging activity of KIOM-79 was 36% at 10 µg/mL, 52% at 50 µg/ mL, and 55% at 100 µg/mL [20], so 50 µg/mL of KIOM-79 was determined to be the optimal dose for the present studies. Cells were seeded on a culture plate at a concentration of 2 × 10 5 cells/mL and were treated with 50 µg/mL KIOM-79 at 16 h after plating.…”

Section: Cytosolic Ca 2+ Measurementmentioning

confidence: 96%

KIOM-79 attenuated cell damage induced by endoplasmic reticulum stress by inhibiting apoptosis in RINm5F cells

Kim

Hyun

2011

Biotechnol Bioproc E

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Endoplasmic reticulum (ER) is a cellular compartment responsible for biosynthesis and folding of newly synthesized proteins destined for secretion, such as insulin. ER stress plays a role in the pathogenesis of diabetes and is associated with pancreatic β-cell damage. The aim of this study was to examine the effect of KIOM-79, a mixture of plant extracts, on streptozotocin (STZ)-induced ER stress in pancreatic RINm5F β-cells. STZ induced characteristics of ER stress; the release of Ca 2+ from ER, increased ER staining, induction of glucose-regulated protein-78, phosphorylation of PKR-like ER kinase, and eukaryotic initiation factor-2α, as well as cleavage of activating transcription factor-6, whereas KIOM-79 inhibited these changes. Moreover, KIOM-79 inhibited STZ-induced apoptotic cell death. STZ induced CCAAT/enhancer-binding protein-homologous protein (CHOP) and cleavage of caspase 12, which are ER stress-induced apoptosis regulatory proteins; however, KIOM-79 suppressed these effects. KIOM-79 suppressed apoptosis induced by STZ treatment in CHOP siRNA-transfected cells. Furthermore, KIOM-79 restored cell viability decreased by STZ treatment via ER-stressed apoptosis. The pancreatic β-cells damaged by STZ had decreased levels of insulin, and KIOM-79 restored the levels. Taken together, these results suggest that KIOM-79 had cytoprotective effects against STZ-induced apoptosis by interrupting the ER stress pathway.

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“…RINm5F cells were selected based on their established use to study cytoprotective effects (Kang et al 2007). Cells were cultured and incubated at 37°C in an atmosphere of 5% CO 2 and 95% air.…”

Section: Cell Culturementioning

confidence: 99%

Hypoglycemic activity of C-glycosyl flavonoid fromEnicostemma hyssopifolium

Patel

Mishra

2011

Pharmaceutical Biology

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Cytoprotective Effects of KIOM-79 on Streptozotocin Induced Cell Damage by Inhibiting ERK and AP-1

Cited by 24 publications

References 39 publications

Gymnema montanum H. Protects Against Alloxan-induced Oxidative Stress and Apoptosis in Pancreatic β-cells

Gymnema montanum H. Protects Against Alloxan-induced Oxidative Stress and Apoptosis in Pancreatic β-cells

KIOM-79 attenuated cell damage induced by endoplasmic reticulum stress by inhibiting apoptosis in RINm5F cells

Hypoglycemic activity of C-glycosyl flavonoid fromEnicostemma hyssopifolium

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