Triterpenoid saponin, oleanolic acid 3-O-β-d-glucopyranosyl(1→3)-α-l-rhamnopyranosyl(1→2)-α-l-arabinopyranoside (OA) from Aralia elata inhibits LPS-induced nitric oxide production by down-regulated NF-κB in raw 264.7 cells

Suh, Sungho; Jin, Un‐Ho; Kim, Kyung-Woon; Son, Jong‐Keun; Lee, Seung Ho; Son, Kun-Ho; Chang, Hyen Wook; Lee, Young Choon; Kim, Cheorl-Ho

doi:10.1016/j.abb.2007.08.025

Cited by 49 publications

(41 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…To elucidate whether A. cordata affects general motor functions, we measured spontaneous locomotor activity and motor coordination in the mice. Neither A. Cordata nor Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) significantly affected locomotor and rota-rod activity (data not shown), indicating that the observed improvement of memory by A. cordata was not due to immobility.…”

Section: A Cordata Inhibits Aβ(25-35)-induced Memory Impairment and mentioning

confidence: 93%

“…In neurons treated with 10 μM Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), the relative fluorescence increased approximately 2.5-fold to 108.8 ± 7.0 compared with the value in control neurons (43.3 ± 2.7; Fig. 6).…”

Section: A Cordata and Oleanolic Acid Inhibit Aβ(25-35)-induced Ros mentioning

confidence: 99%

“…Passive avoidance task: On day 1, A. cordata, donepezil (generously provided by Eisai Co., Ltd., Tokyo), and verapamil were administered to 5-week-old ICR mice and 30 min later, the aggregated form of Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) was administered i.c.v. using a microsyringe with a 27-gauge stainless-steel needle (Hamilton, Reno, NV, USA), the tip of which had been adjusted to a depth of 3 mm.…”

Section: Examination Of Learning and Memorymentioning

confidence: 99%

“…The final concentration of DMSO was ≤0.1%, which did not affect cell viability. For each experiment, A. cordata, oleanolic acid, N G -nitro-L-arginine methyl ester (L-NAME; Sigma), (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801; RBI, Natick, MA, USA), and verapamil (Sigma) were applied 15 min prior to treatment with 10 μM Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). They were also present in the medium during Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) incubation.…”

Section: Induction Of Neurotoxicity In Primary Cultures Of Rat Cerebrmentioning

confidence: 99%

“…Also, α-tocopherol and anti-inflammatory agents such as indomethacin reportedly slow the progression of AD (13,14). Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), the core toxic fragment of Aβ , produces similar neurodegenerative properties as Aβ , including oxidative damage, inflammatory responses, and memory impairment (15,16). Aralia species belong to the family Araliaceae and have long been recognized in China, Japan, and Korea as therapeutic herbs with antinociceptive, antidiabetic, antioxidant, and anti-inflammatory activities.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Aralia cordata Protects Against Amyloid β Protein (25–35)–Induced Neurotoxicity in Cultured Neurons and Has Antidementia Activities in Mice

et al. 2009

View full text Add to dashboard Cite

Abstract. The present study investigated an ethanol extract of the aerial part of Aralia cordata Thunb. (Araliaceae) for possible neuroprotective effects on neurotoxicity induced by amyloid β (Aβ) protein (25 -35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to 10 μM Aβ(25 -35) for 36 h induced neuronal apoptotic death. At 1 -10 μg/ml, A. cordata inhibited neuronal death, elevation of intracellular calcium ([Ca 2+ ] i ), glutamate release into the medium, and generation of reactive oxygen species (ROS) induced by in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol Aβ(25-35) was inhibited by chronic treatment with A. cordata (50 and 100 mg/kg, p.o. for 7 days) as measured by a passive avoidance test, and corresponding reductions were observed in brain cholinesterase activity and neuronal death measured histologically in the hippocampal region. Oleanolic acid isolated from A. cordata also inhibited neuronal death, elevation of [Ca 2+ ] i , glutamate release, and generation of ROS induced by Aβ(25-35) in cultured rat cortical neurons, suggesting that the neuroprotective effect of A. cordata may be, at least in part, attributable to this compound. From these results, we suggest that the antidementia effect of A. cordata is due to its neuroprotective effect against Aβ(25-35)-induced neurotoxicity and that A. cordata may have a therapeutic role in preventing the progression of Alzheimer's disease.

show abstract

Section: A Cordata Inhibits Aβ(25-35)-induced Memory Impairment and mentioning

confidence: 93%

Section: A Cordata and Oleanolic Acid Inhibit Aβ(25-35)-induced Ros mentioning

confidence: 99%

Section: Examination Of Learning and Memorymentioning

confidence: 99%

Section: Induction Of Neurotoxicity In Primary Cultures Of Rat Cerebrmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Aralia cordata Protects Against Amyloid β Protein (25–35)–Induced Neurotoxicity in Cultured Neurons and Has Antidementia Activities in Mice

et al. 2009

View full text Add to dashboard Cite

show abstract

The molecular mechanisms underpinning the therapeutic properties of oleanolic acid, its isomer and derivatives for type 2 diabetes and associated complications

Camer

Szabo

et al. 2014

Molecular Nutrition Food Res

View full text Add to dashboard Cite

X. (2014). The molecular mechanisms underpinning the therapeutic properties of oleanolic acid, its isomer and derivatives for type 2 diabetes and associated complications. Molecular Nutrition and Food Research, 58 (8), 1750-1759. The molecular mechanisms underpinning the therapeutic properties of oleanolic acid, its isomer and derivatives for type 2 diabetes and associated complications AbstractRecent research has uncovered the molecular mechanisms responsible for the therapeutic properties of oleanolic acid (OA), its isomer ursolic acid (UA), and derivatives. In particular, recent reports have highlighted the benefits of these compounds in the prevention and treatment of type 2 diabetes and associated life-threatening complications, such as nonalcoholic fatty liver disease, nephropathy, retinopathy, and atherosclerosis. The prevalence of type 2 diabetes is of major concern since it is reaching global epidemic levels. Treatments targeting the signaling pathways altered in type 2 diabetes are being actively investigated, and OA and UA in natural and derivative forms are potential candidates to modulate these pathways. We will explore the findings from in vitro and in vivo studies showing that these compounds: (i) improve insulin signaling and reduce hyperglycemia; (ii) reduce oxidative stress by upregulating anti-oxidants and; (iii) reduce inflammation by inhibiting proinflammatory signaling. We will discuss the molecular mechanisms underpinning these therapeutic properties in this review in order to provide a rationale for the future use of OA, UA, and their derivatives for the prevention and treatment of type 2 diabetes and associated comorbidities. Abstract: Recent research has uncovered the molecular mechanisms responsible for the therapeutic properties of oleanolic acid (OA), its isomer ursolic acid (UA) and derivatives. In particular, recent reports have highlighted the benefits of these compounds in the prevention and treatment of type 2 diabetes and associated life-threatening complications, such as nonalcoholic fatty liver disease, nephropathy, retinopathy and atherosclerosis. The prevalence of type 2 diabetes is of major concern since it is reaching global epidemic levels. Treatments targeting the signalling pathways altered in type 2 diabetes are being actively investigated, and OA and UA in natural and derivative forms are potential candidates to modulate these pathways. We will explore the findings from in vitro and in vivo studies showing that these compounds: 1) Improve insulin signalling and reduce hyperglycaemia; 2) Reduce oxidative stress by upregulating anti-oxidants and; 3) Reduce inflammation by inhibiting proinflammatory signalling. We will discuss the molecular mechanisms underpinning these therapeutic properties in this review in order to provide a rationale for the future use of OA, UA and their derivatives for the prevention and treatment of type 2 diabetes and associated comorbidities.

show abstract

Oleanolic acid alleviated pressure overload-induced cardiac remodeling

et al. 2015

View full text Add to dashboard Cite

Previous study has demonstrated that oleanolic acid (OA) possessing the anti-inflammatory and anti-oxidant properties blunted high-glucose-induced diabetic cardiomyopathy and ameliorated experimental autoimmune myocarditis in mice. However, little is known about its effects on pressure overload-induced cardiac remodeling. Herein, we investigated the effect of OA on cardiac remodeling and underlying mechanism. Mice, subjected to aortic banding (AB), were randomly assigned into control group and experimental group. OA premixed in diets was administered to mice after 3 days of AB. Echocardiography and catheter-based measurements of hemodynamic parameters were performed after 8 weeks' treatment of OA. Histologic examination and molecular analyses were used to assess cardiac hypertrophy and tissue fibrosis. In addition, the inhibitory effects of OA on H9c2 cardiomyocytes and cardiac primary fibroblast responded to the stimulation of AngII were also investigated. OA ameliorated the systolic and diastolic dysfunction induced by pressure overload evidenced by echocardiography and catheter-based measurements. OA also decreased the mRNA expression of cardiac hypertrophy and fibrosis markers evidenced by RT-PCR. It has been shown in our study that pressure overload activated the phosphorylations of Akt, mTOR, p70s6k, S6, GSK3β, and FoxO3a, and treatment of OA attenuated the phosphorylation of these proteins. In addition, hypertrophy of cardiomyocytes and fibrosis markers induced by AngII was inhibited by OA in vitro. Our findings uncover that OA suppressed AB-induced cardiac hypertrophy, partly by inhibiting the activity of Akt/mTOR pathway, and suggest that treatment of OA may have a benefit on retarding the progress of cardiac remodeling under long terms of pressure overload.

show abstract

Triterpenoid saponin, oleanolic acid 3-O-β-d-glucopyranosyl(1→3)-α-l-rhamnopyranosyl(1→2)-α-l-arabinopyranoside (OA) from Aralia elata inhibits LPS-induced nitric oxide production by down-regulated NF-κB in raw 264.7 cells

Cited by 49 publications

References 44 publications

Aralia cordata Protects Against Amyloid β Protein (25–35)–Induced Neurotoxicity in Cultured Neurons and Has Antidementia Activities in Mice

Aralia cordata Protects Against Amyloid β Protein (25–35)–Induced Neurotoxicity in Cultured Neurons and Has Antidementia Activities in Mice

The molecular mechanisms underpinning the therapeutic properties of oleanolic acid, its isomer and derivatives for type 2 diabetes and associated complications

Oleanolic acid alleviated pressure overload-induced cardiac remodeling

Contact Info

Product

Resources

About