Effect of Aralia cordata extracts on cartilage protection and apoptosis inhibition.
(9/15)
Cartilage loss in osteoarthritis is characterized by cartilage degradation and chondrocyte death. Cartilage degradation is induced by activation of matrix-metalloproteinases (MMPs) activity and degradation of glycosaminoglycan (GAG) and collagen. Also, chondrocyte death is induced by the apoptosis through the activation of MAP kinase and caspases activities. On the basis of this background, our study was designed to examine the cartilage protective and anti-apoptotic effect of Aralia cordata. Cartilage explants and Chondrocytes were cultured from rabbit knee joint cartilage and treated by 5 ng/ml IL-1alpha. Cartilage and chondroprotective effects of Aralia cordata were determined by measuring (1) GAG and collagen expression, (2) GAG and collagen degradation, (3) TIMP and MMPs expression, and (4) TIMP and MMPs activity. Anti-apoptotic effects of Aralia cordata were determined by measuring (1) JNK and p38 MAP kinase expression, (2) apoptotic cells by flow cytometry, and (3) caspase-3 activity. In cartilage explants and chondroctyes treated by IL-1alpha, Aralia cordata showed the decrease of GAG and collagen degradation, decrease of MMPs (MMP-1, -3, -13) activity, and increase of TIMP-1 activity in a dose-dependent manner. Aralia cordata also showed anti-apoptotic effect by inhibition of early and late apoptotic cells, sub-G1 phase cells, and caspase-3 activity through the downregulation of JNK and p38 MAP kinase signaling pathway. Aralia cordata inhibited the cartilage and chondrocyte destruction through the downregulation of MMPs activities and the inhibition of proteoglycan and collagen degradation. Also, Aralia cordata inhibited the chondrocyte apoptosis through the downregulation of JNK and p38 MAP kinase signal, and the inhibition of caspase-3 activity. (+info)
Anticancer effect of extracts from a North American medicinal plant--wild sarsaparilla.
(10/15)
The wild sarsaparilla (Aralia nudicaulis) plant is richly distributed in North America, mainly in Canada. In the present study, 24 extracts were obtained from the rhizome, stem, leaf and fruit of wild sarsaparilla. In the presence of RH (hexane fraction from the rhizome), the survival rate of WiDr (human colon cancer cell) was 3.5 +/- 2.7% (IC50 = 30.1 +/- 3.5 microg/ml) and that of Molt (human leukemia cell) was 2.4 +/- 2.8% (IC50 = 7.0 +/- 0.6 microg/ml). The survival rate of HELA (human cervix cancer cell) was only 1.8 +/- 0.9% in the presence of FH (hexane fraction from the fruit of wild sarsaparilla) (IC50 = 33.3 +/- 2.7 microg/ml). The cytotoxicities of RH and FH against normal human umbilical vein endothelial cells were significantly lower than against the tested human cancer cells. RH appeared to be the best extract against WiDr and Molt, whereas FH was the most effective against HELA. Because of the rich natural supply, simple extraction procedure and high yield, RH and FH of wild sarsaparilla have the potential to be developed into selective anticancer nutraceutical and/or pharmaceutical products with few side-effects and low cost. (+info)
Protective effect of total aralosides of Aralia elata (Miq) Seem (TASAES) against diabetic cardiomyopathy in rats during the early stage, and possible mechanisms.
(11/15)
Analysis of saponins from leaves of Aralia elata by liquid chromatography and multi-stage tandem mass spectrometry.
(12/15)
Four saponins were isolated from the leaves of Aralia elata, and established using NMR and other spectroscopic methods, as well as data reported in the literature. Three Aralia saponins from the leaves of Aralia elata sharing the same structures as those isolated from the root bark suggested that the leaves would be a good substitute for the root bark of Aralia elata. These four Aralia saponins were then extensively investigated using complementarily positive and negative electrospray ionization multistage tandem mass spectrometry (ESI-MS(n)). Two isomers of saponins with different sugar linkages were then successfully differentiated by positive ESI-MS(n) and verified with different retention times and the collision-induced dissociation (CID) spectra by LC-MS. A simple and effective LC-MS method was thus developed for the rapid identification and screening of these saponins in plant extracts from leaves of Aralia elata. (+info)
Aralia cordata protects against amyloid beta protein (25-35)-induced neurotoxicity in cultured neurons and has antidementia activities in mice.
(13/15)
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 beta (Abeta) protein (25 - 35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to 10 muM Abeta(25 - 35) for 36 h induced neuronal apoptotic death. At 1 - 10 mug/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 Abeta(25-35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol Abeta(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 Abeta(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 Abeta(25-35)-induced neurotoxicity and that A. cordata may have a therapeutic role in preventing the progression of Alzheimer's disease. (+info)
ent-kaur-16-en-19-oic Acid, isolated from the roots of Aralia continentalis, induces activation of Nrf2.
(14/15)