The Experts below are selected from a list of 1119 Experts worldwide ranked by ideXlab platform
Meichin Yin - One of the best experts on this subject based on the ideXlab platform.
-
Asiatic Acid and maslinic Acid attenuated kainic Acid induced seizure through decreasing hippocampal inflammatory and oxidative stress
Epilepsy Research, 2018Co-Authors: Zhi-hong Wang, Mei-chin Mong, Meichin Yin, Yachen YangAbstract:Seizure is a neurological disorder including hippocampal oxidative and inflammatory stress, and glutamate toxicity. Thus, any agent(s) that mitigate(s) these events in hippocampus might attenuate seizure severity. The effects of Asiatic Acid (AA) or maslinic Acid (MA) pre-administration at 20 or 40mg/kg body weight/day upon inflammatory, oxidative and apoptotic injury in hippocampus of kainic Acid (KA)-treated mice were examined. KA induced seizure-like behavioral patterns, which was attenuated by AA or MA pre-administration. KA stimulated the release of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha and prostaglandin E2 in hippocampus of mice. AA or MA pre-administration decreased the production of these inflammatory factors. AA or MA also diminished KA-induced increase in hippocampal cyclooxygenase-2 activity and relative NF-κB p50/65 binding activity. KA depleted glutathione content and promoted reactive oxygen species generation. AA or MA pre-administration reversed these alterations. KA lowered Bcl-2 mRNA expression and increased Bax mRNA expression. AA or MA treatments reduced Bax mRNA expression. AA or MA pre-administration enhanced glutamine synthetase activity, decreased glutamate level and increased glutamine level in hippocampus of KA treated mice. In addition, AA or MA pre-treatments at 10 and 20μM increased viability and decreased plasma membrane damage in KA treated nerve growth factor (NGF)-differentiated PC12 cells. Both agents also lowered the release of calcium ion induced by KA in NGF-treated PC12 cells. These findings support that Asiatic Acid and maslinic Acid are potent nutraceutical agents for seizure alleviation.
-
Asiatic Acid attenuated apoptotic and inflammatory stress in the striatum of mptp treated mice
Food & Function, 2016Co-Authors: Peichun Chao, Hsianglin Lee, Meichin YinAbstract:The effects of post-treatments with Asiatic Acid (AA) at 20, 40 or 80 mg per kg BW per day against apoptotic, oxidative and inflammatory injury in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice were examined. The results showed that AA supplements at 40 and 80 mg per kg BW per day increased AA deposit in the striatum, increased glutathione content and decreased reactive oxygen species production in the striatum. AA supplements at 20–80 mg per kg BW per day dose-dependently lowered striatal levels of nitric oxide, 3-nitrotyrosine, interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha and prostaglandin E2. AA supplements at 40 and 80 mg per kg BW per day down-regulated striatal p47phox and gp91phox expression; but, at three test doses suppressed striatal expression of inducible nitric oxide synthase and cyclooxygenase-2. AA post-treatments at 40 and 80 mg per kg BW per day enhanced Bcl-2 expression, and lowered Bax, apoptosis-inducing factor and caspase-3 expression in the striatum. AA at 20–80 mg per kg BW per day up-regulated striatal tyrosine hydroxylase expression, and suppressed Toll-like receptors (TLR)2 and nuclear factor kappa B p65 expression. AA treatments at 40 and 80 mg per kg BW per day decreased striatal expression of α-synuclein and TLR4, increased striatal levels of dopamine, brain-derived nerve growth factor and glial cell line-derived neurotrophic factor. These novel findings suggest that Asiatic Acid is a potent nutraceutical agent against the progression of Parkinson's disease.
-
antioxidative and antiinflammatory activities of Asiatic Acid glycyrrhizic Acid and oleanolic Acid in human bronchial epithelial cells
Journal of Agricultural and Food Chemistry, 2015Co-Authors: Shihming Tsao, Meichin YinAbstract:Protective effects of triterpenic Acids, Asiatic Acid (AA), glycyrrhizic Acid (GA), or oleanolic Acid (OA), for two human bronchial epithelial cells, 16HBE and BEAS-2B cells, against hydrogen peroxide (H2O2) induced injury were examined. Cells were pretreated by triterpenic Acid at 4 or 8 μmol/L and followed by H2O2 treatment. Results showed that H2O2 significantly upregulated both Bax and cleaved caspase-3 expression, and also downregulated Bcl-2 expression in test cells. AA at these doses retained Bcl-2 expression, but GA and OA only at 8 μmol/L reserved Bcl-2 expression. Test triterpenic Acids lowered cleaved caspase-3 expression dose-dependently. H2O2 treatment lowered Na+-K+-ATPase activity and mitochondrial membrane potential in cells. Triterpenic Acid pretreatments significantly maintained mitochondrial membrane potential and Na+-K+-ATPase activity. H2O2 enhanced reactive oxygen species, interleukin-6, tumor necrosis factor-α, and prostaglandin E2 levels in test cells. Three triterpenic Acid treatm...
-
retraction of antioxidative and antiinflammatory activities of Asiatic Acid glycyrrhizic Acid and oleanolic Acid in human bronchial epithelial cells
Journal of Agricultural and Food Chemistry, 2015Co-Authors: Shihming Tsao, Meichin YinAbstract:Protective effects of triterpenic Acids, Asiatic Acid (AA), glycyrrhizic Acid (GA), or oleanolic Acid (OA), for two human bronchial epithelial cells, 16HBE and BEAS-2B cells, against hydrogen peroxide (H2O2) induced injury were examined. Cells were pretreated by triterpenic Acid at 4 or 8 μmol/L and followed by H2O2 treatment. Results showed that H2O2 significantly upregulated both Bax and cleaved caspase-3 expression, and also downregulated Bcl-2 expression in test cells. AA at these doses retained Bcl-2 expression, but GA and OA only at 8 μmol/L reserved Bcl-2 expression. Test triterpenic Acids lowered cleaved caspase-3 expression dose-dependently. H2O2 treatment lowered Na+-K+-ATPase activity and mitochondrial membrane potential in cells. Triterpenic Acid pretreatments significantly maintained mitochondrial membrane potential and Na+-K+-ATPase activity. H2O2 enhanced reactive oxygen species, interleukin-6, tumor necrosis factor-α, and prostaglandin E2 levels in test cells. Three triterpenic Acid treatm...
-
Asiatic Acid ameliorates hepatic lipid accumulation and insulin resistance in mice consuming a high fat diet
Journal of Agricultural and Food Chemistry, 2014Co-Authors: Sheng Lei Yan, Meichin Yin, Hui Ting Yang, Yiju Lee, Chunche Lin, Ming Hui ChangAbstract:Effects of Asiatic Acid (AA) at 10 or 20 mg/kg/day upon hepatic steatosis in mice consuming a high-fat diet (HFD) were examined. AA intake decreased body weight, water intake, feed intake, epididymal fat, and plasma and hepatic triglyceride levels in HFD-treated mice (P < 0.05). HFD enhanced 2.85-fold acetyl coenzyme A carboxylase (ACC1), 3.34-fold fatty Acid synthase (FAS), 3.71-fold stearoyl CoA desaturase (SCD)-1, 3.62-fold 3-hydroxy-3-methylglutaryl coenzyme A reductase, 2.91-fold sterol regulatory element-binding protein (SREBP)-1c, and 2.75-fold SREBP-2 expression in liver (P < 0.05). Compared with HFD groups, AA intake at two doses reduced 18.9–45.7% ACC1, 25.1–49.8% FAS, 24.7–57.1% SCD-1, and 21.8–53.3% SREBP-1c protein expression (P < 0.05). Histological results indicated AA intake at two doses reduced hepatic lipid accumulation and inflammatory infiltrate. HFD increased hepatic production of reactive oxygen species, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, as well as decreased hep...
Jing Gao - One of the best experts on this subject based on the ideXlab platform.
-
Asiatic Acid Prevents Oxidative Stress and Apoptosis by Inhibiting the Translocation of α-Synuclein Into Mitochondria
'Frontiers Media SA', 2018Co-Authors: Hongqun Ding, Yuyun Xiong, Jing Sun, Chen Chen, Jing GaoAbstract:The association of α-synuclein (α-syn) with mitochondria occurs through interaction with mitochondrial complex I. Defects in this protein have been linked to the pathogenesis of Parkinson disease (PD). Overexpression of α-synuclein in cells has been suggested to cause elevations in mitochondrial oxidant radicals and structural and functional abnormalities in mitochondria. Asiatic Acid (AA), a triterpenoid, is an antioxidant that is used for depression, and we have shown that pretreatment with AA can prevent PD-like damage, but its therapeutic effects in PD and mechanism remain unknown. In this study, we found that 0.5–2 mg AA/100 g diet significantly improves climbing ability in drosophila and extends their life-span—effects that we attributed to its antioxidant properties. AA also protected mitochondria against oxidative stress and apoptosis in a rotenone-induced cellular model. In an isolated mitochondria model, AA attenuated the decline in mitochondrial membrane potential that was induced by α-syn. Consequently, AA maintained membrane integrity and ATP production. Finally, we demonstrated that AA protects by blocking the translocation of α-syn into mitochondria. Our results suggest that mitochondria are crucial in PD and that AA is an excellent candidate for the prevention and therapy of this disease
-
Asiatic Acid uncouples respiration in isolated mouse liver mitochondria and induces hepg2 cells death
European Journal of Pharmacology, 2016Co-Authors: Siyuan Liu, Jing Gao, Ying Wang, Dang Wang, Li ZhuAbstract:Asiatic Acid, one of the triterpenoid components isolated from Centella Asiatica, has received increasing attention due to a wide variety of biological activities. To date, little is known about its mechanisms of action. Here we examined the cytotoxic effect of Asiatic Acid on HepG2 cells and elucidated some of the underlying mechanisms. Asiatic Acid induced rapid cell death, as well as mitochondrial membrane potential (MMP) dissipation, ATP depletion and cytochrome c release from mitochondria to the cytosol in HepG2 cells. In mitochondria isolated from mouse liver, Asiatic Acid treatment significantly stimulated the succinate-supported state 4 respiration rate, dissipated the MMP, increased Ca(2+) release from Ca(2+)-loaded mitochondria, decreased ATP content and promoted cytochrome c release, indicating the uncoupling effect of Asiatic Acid. Hydrogen peroxide (H2O2) produced by succinate-supported mitochondrial respiration was also significantly inhibited by Asiatic Acid. In addition, Asiatic Acid inhibited Ca(2+)-induced mitochondrial swelling but did not induce mitochondrial swelling in hyposmotic potassium acetate medium which suggested that Asiatic Acid may not act as a protonophoric uncoupler. Inhibition of uncoupling proteins (UCPs) or blockade of adenine nucleotide transporter (ANT) attenuated the effect of Asiatic Acid on MMP dissipation, Ca(2+) release, mitochondrial respiration and HepG2 cell death. When combined inhibition of UCPs and ANT, Asiatic Acid-mediated uncoupling effect was noticeably alleviated. These results suggested that both UCPs and ANT partially contribute to the uncoupling properties of Asiatic Acid. In conclusion, Asiatic Acid is a novel mitochondrial uncoupler and this property is potentially involved in its toxicity on HepG2 cells.
-
Asiatic Acid ameliorates dextran sulfate sodium induced murine experimental colitis via suppressing mitochondria mediated nlrp3 inflammasome activation
International Immunopharmacology, 2015Co-Authors: Wenjie Guo, Wen Liu, Biao Jin, Ji Geng, Hongqun Ding, Yang Sun, Jing GaoAbstract:In the present study, the effect of Asiatic Acid, a natural triterpenoid compound, on murine experimental colitis induced by dextran sulfate sodium (DSS) and its possible mechanism were examined in vivo and vitro. Oral administration of Asiatic Acid dose-dependently attenuated the loss of body weight and shortening of colon length induced by DSS. The disease activity index, histopathologic scores of musco and myeloperoxidase activity were also significantly reduced by Asiatic Acid treatment. Protein and mRNA levels of DSS-induced pro-inflammatory cytokines in colon, including TNF-α, IL-1β, IL-6 and IFN-γ, were markedly suppressed by Asiatic Acid. At the same time, decreased activation of caspase-1 in peritoneal macrophages was detected in Asiatic Acid-treated mice, which suggested that the NLRP3 inflammasome activation was suppressed. In addition, we also found that Asiatic Acid dose-dependently inhibited IL-1β secretion, caspase-1 activation as well as inflammasome assembling in vitro. Furthermore, the mechanism of Asiatic Acid was related to the inhibition of mitochondrial reactive oxygen species generation and prevention of mitochondrial membrane potential collapse. Taken together, our results demonstrate the ability of Asiatic Acid to inhibit NLRP3 inflammasome activation and its potential usage in the treatment of inflammatory bowel diseases.
-
Asiatic Acid a pentacyclic triterpene in centella Asiatica attenuates glutamate induced cognitive deficits in mice and apoptosis in sh sy5y cells
Acta Pharmacologica Sinica, 2012Co-Authors: Yuyun Xiong, Jiankang Liu, Jinjun Qian, Li Zhu, Jing GaoAbstract:Asiatic Acid, a pentacyclic triterpene in Centella Asiatica , attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells
-
mechanism underlying mitochondrial protection of Asiatic Acid against hepatotoxicity in mice
Journal of Pharmacy and Pharmacology, 2010Co-Authors: Jing Gao, Jin Chen, Xinhui Tang, Liya Pan, Feng Fang, Xiaoning ZhaoAbstract:Asiatic Acid (AA) is one of the triterpenoid components of Terminalia catappa L., which has antioxidative, anti-inflammatory and hepatoprotective activity. This research focused on the mitochondrial protection of AA against acute liver injury induced by lipopolysaccharide (LPS) and D-galactosamine (D-GalN) in mice. It was found that pretreatment with 25, 50 or 100 mg kg(-1) AA significantly blocked the LPS + D-GalN-induced increase in both serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT) levels, which was confirmed by ultrastructural observation under an electron microscope, showing improved nuclear condensation, ameliorated mitochondrion proliferation and less lipid deposition. Meanwhile, different doses of AA could decrease both the transcription and the translation level of voltage-dependent anion channels (VDACs), the most important mitochondrial PTP component protein, and block the translocation of cytochrome c from mitochondria to cytosol. On the other hand, pre-incubation with 25, 50 and 100 microg mL(-1) AA inhibited the Ca(2+)-induced mitochondrial permeability transition (MPT), including mitochondrial swelling, membrane potential dissipation and releasing of matrix Ca(2+) in liver mitochondria separated from normal mice, indicating the direct role of AA on mitochondria. Collectively, the above data suggest that AA could protect liver from damage and the mechanism might be related to up-regulating mitochondrial VDACs and inhibiting the process of MPT.
Yisong Qian - One of the best experts on this subject based on the ideXlab platform.
-
Asiatic Acid suppresses neuroinflammation in bv2 microglia via modulation of the sirt1 nf κb signaling pathway
Food & Function, 2017Co-Authors: Yisong Qian, Zhaochen Xin, Ziwei Wang, Li Zuo, Xiang Huang, Hongbo XinAbstract:Asiatic Acid, a triterpenoid derived from Centella Asiatica, has been found to exhibit multiple bioactivities. In this study, we investigated the effects of Asiatic Acid on lipopolysaccharide (LPS)-induced neuroinflammation and explored the mechanism of its action in BV2 microglia. We found that Asiatic Acid (0.1 to 100 μM) treatment significantly attenuated nitric oxide (NO) production and inhibited inducible nitric oxide synthase (iNOS) expression in a concentration-dependent manner following LPS exposure. Asiatic Acid reduced LPS-induced expression and secretion of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in BV2 cells. In addition, Asiatic Acid enhanced Sirt1 expression, reduced NF-κB p65 acetylation, and suppressed NF-κB activation after LPS stimulation. However, EX-527, an inhibitor of Sirt1, abolished the inhibitory effects of Asiatic Acid on LPS-stimulated microglia activation. These findings suggest that Asiatic Acid prevents LPS-induced neuroinflammation via regulating the Sirt1/NF-κB signaling pathway.
-
Asiatic Acid attenuates myocardial ischemia reperfusion injury via akt gsk 3β hif 1α signaling in rat h9c2 cardiomyocytes
Molecules, 2016Co-Authors: Xiang Huang, Li Zuo, Hongbo Xin, Chuqiao Chen, Yaqin Yang, Yisong QianAbstract:Myocardial ischemic/reperfusion injury results from severe impairment of coronary blood supply and leads to irreversible cell death, with limited therapeutic possibilities. Asiatic Acid is a pentacyclic triterpenoid derived from the tropical medicinal plant Centella Asiatica and serves a variety of bioactivities. In this study, we determined the effect of Asiatic Acid on myocardial ischemia/reperfusion injury and investigated the underlying mechanisms, using an in vitro rat H9c2 cardiomyocytes model of oxygen-glucose deprivation/reoxygenation (OGD/R) injury. Results showed that pre-treatment with Asiatic Acid significantly augmented cell viability and prevented lactate dehydrogenase (LDH) release in a concentration-dependent manner after OGD/R exposure. Asiatic Acid at 10 μM effectively inhibited apoptotic cell death, suppressed the activities of caspase-3 and caspase-9, and reversed Bax/Bcl-2 ratio in hypoxic H9c2 cells. In addition, Asiatic Acid improved mitochondrial function, as evidenced by reduced reactive oxygen species (ROS) accumulation, enhanced mitochondrial membrane potential and decreased intracellular calcium concentration. Using Western blot assay, we found that Asiatic Acid promoted the phosphorylation of Akt and subsequent inactivation of glycogen synthase kinase-3β (GSK-3β), and induced the expression of hypoxia-inducible factor 1α (HIF-1α) after OGD/R. The cardioprotective effects of Asiatic Acid were attenuated by the Akt or HIF-1α inhibitor. Taken together, these data suggested that Asiatic Acid exerted protective effects against OGD/R-induced apoptosis in cardiomyocytes, at least partly via the Akt/GSK-3β/HIF-1α pathway.
Eungseok Lee - One of the best experts on this subject based on the ideXlab platform.
-
Modification of C2 functional group on Asiatic Acid and the evaluation of hepatoprotective effects
Archives of Pharmacal Research, 2007Co-Authors: Byeongseon Jeong, Young Choong Kim, Mi Kyeong Lee, Eungseok LeeAbstract:For the development of novel hepatoprotective agents, C2 functional group on Asiatic Acid was modified, and evaluated for their hepatoprotective effects. Among prepared compounds, com-pounds 10 and 14 showed better hepatoprotective effects compared to Silymarin.
-
modification of c2 3 23 28 functional groups on Asiatic Acid and evaluation of hepatoprotective effects
Bulletin of The Korean Chemical Society, 2007Co-Authors: Byeongseon Jeong, Young Choong Kim, Eungseok LeeAbstract:we found that simple modification of functionalgroups on C2, C3, C23 or C28 groups on Asiatic Acid greatlyaffected the hepatoprotective activities. It would be veryinteresting to prepare the modified derivatives on C2, C3,C23 and C28 functional groups on Asiatic Acid and evaluatehepatoprotective effects of the prepared compounds. Inaddition, structure-activity relationship studies of the pre-pared derivatives may provide valuable information for thedevelopment of novel hepatoprotective agents. In connec-tion with previous studies, C2, C3, C23 and C28 functionalgroups on Asiatic Acid were modified and evaluated for theirhepatoprotective effects.
-
inhibitory effects of Asiatic Acid on 7 12 dimethylbenz a anthracene and 12 o tetradecanoylphorbol 13 acetate induced tumor promotion in mice
Biological & Pharmaceutical Bulletin, 2007Co-Authors: Byung Chul Park, Eungseok Lee, Seunghwan Paek, Yoonseok Lee, Seung Joo Kim, Hangon Choi, Chul Soon Yong, Jungae KimAbstract:Asiatic Acid, a pentacyclic triterpene, has been reported to induce apoptosis of various human cancer cells. In the present study, we assessed the anti-tumor promoting effect of Asiatic Acid against 12-O-tetradecanoylphorbol 13-acetate (TPA)-mediated skin tumorigenesis in 7,12-dimethylbenz[a]anthracene (DMBA)-initiated ICR mice. Topical application of Asiatic Acid prior to each application of TPA resulted in a significant reduction in skin tumor formation. We also found that pre-application of Asiatic Acid alleviated TPA-induced [3H]thymidine incorporation, which is a conventional marker for skin tumor promotion. In addition, Asiatic Acid inhibited the TPA-induced generation of nitric oxide (NO) and expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), which are known to play important roles in tumor growth, especially in the promotion stage. In addition, topical application of aminoguanidine (AG), a selective iNOS inhibitor, and N(G)-nitro-L-arginine-methyl ester (NAME), another iNOS inhibitor, 30 min prior to TPA treatment significantly inhibited the TPA-induced COX-2 expression. These results suggest that Asiatic Acid may exert anti-tumorigenesis through inhibitory actions in NO and COX-2 signals.
-
modification of c11 c28 c2 3 23 or c2 23 28 functional groups on Asiatic Acid and evaluation of hepatoprotective effects
Bulletin of The Korean Chemical Society, 2007Co-Authors: Longxuan Zhao, Sangsup Jew, Hyeunggeun Park, Byeongseon Jeong, Young Choong Kim, Mi Kyeong Lee, Pritam Thapa, Radha Karki, Yurngdong Jahng, Eungseok LeeAbstract:For the development of novel hepatoprotective agents, C11, C28, C2,3,23 or C2,23,28 functional groups on Asiatic Acid were modified, and their hepatoprotective effects were evaluated. Most of the prepared compounds displayed potent hepatoprotective activities against CCl 4- and galactosamine (GaIN)-induced hepatotoxicity. Especially, compounds 16 and 20 showed the most significant hepatoprotective effects against GaIN-induced hepatotoxicity (54.2% and 46.4% protection at 50 mM, respectively).
-
Asiatic Acid induces apoptosis in sk mel 2 human melanoma cells
Cancer Letters, 2005Co-Authors: Byung Chul Park, Eungseok Lee, Yong Soo Lee, Kefa O Bosire, Jungae KimAbstract:Asiatic Acid (AA) is a pentacyclic triterpene found in Centella Asiatica. In the present study, the mechanism of anticancer effect of AA on skin cancer was investigated. AA decreased viability and induced apoptosis in human melanoma SK-MEL-2 cells in a time- and dose-dependent manner. AA also markedly increased intracellular reactive oxygen species (ROS) level and enhanced the expression of Bax but not Bcl-2 protein in the cells. In addition, AA-induced activation of caspase-3 activity in a dose-dependent manner. Pretreatment with Trolox, an antioxidant, significantly blocked the induction of Bax and activation of caspase-3 in AA-treated cells. Furthermore, Ac-DEVD-CHO, a specific caspase-3 inhibitor, and Trolox prevented the AA-induced apoptosis. AA did not elevate p53 nuclear protein levels that are present in a mutant form in SK-MEL-2 cells. These results suggest that AA-induced apoptosis may be mediated through generation of ROS, alteration of Bax/Bcl-2 ratio and activation of caspase-3, but p53-independent. These results further suggest that AA may be a good candidate for the therapeutic intervention of human skin cancer.
Hyunju Jung - One of the best experts on this subject based on the ideXlab platform.
-
Asiatic Acid induces colon cancer cell growth inhibition and apoptosis through mitochondrial death cascade
Biological & Pharmaceutical Bulletin, 2009Co-Authors: Xuelian Tang, Xinying Yang, Hyunju Jung, Sungyeon Kim, Sukyul Jung, Duyoung Choi, Woncheol Park, Hyun ParkAbstract:Cancer is one of the leading causes of death in the world. The triterpenoid compound Asiatic Acid derived from the tropical medicinal plant Centella Asiatica displays cytotoxic activity on fibroblast cells and several other kinds of cells. The present work studies Asiatic Acid-mediated growth inhibition of cancer cells and the underlying mechanism. Asiatic Acid markedly inhibited cancer cell proliferation. Apoptosis of SW480 human colon cancer cells was induced by Asiatic Acid as shown by flow cytometry, DNA fragmentation and nuclear chromatin condensation experiments. Through increasing mitochondrial membrane permeability and cytochrome c release from mitochondria into cytosol, Asiatic Acid induced caspase-9 activity, which further activated caspase-3 and poly(ADP-ribose) polymerase cleavage resulting in irreversible apoptotic death in the tumor cells. Taken together, these results suggest that mitochondrial death apoptosis cascade plays very important roles in Asiatic Acid-induced cancer apoptosis.
-
inhibition of lps induced no and pge2 production by Asiatic Acid via nf κb inactivation in raw 264 7 macrophages possible involvement of the ikk and mapk pathways
International Immunopharmacology, 2008Co-Authors: Seo Young Jeong, Heejuhn Park, Hyunju JungAbstract:Abstract In the present study, we investigated the effect of Asiatic Acid (the aglycon of Asiaticoside) and Asiaticoside isolated from the leaves of Centella Asiatica (Umbelliferae) on LPS-induced NO and PGE 2 production in RAW 264.7 macrophage cells. Asiatic Acid more potently inhibited LPS-induced NO and PGE 2 production than Asiaticoside. Consistent with these observations, the protein and mRNA expression levels of inducible iNOS and COX-2 enzymes were inhibited by Asiatic Acid in a concentration-dependent manner. In addition, Asiatic Acid dose-dependently reduced the production of IL-6, IL-1β and TNF-α in LPS-stimulated RAW 264.7 macrophage cells. Furthermore, Asiatic Acid inhibited the NF-κB activation induced by LPS, and this was associated with the abrogation of IκB-α degradation and with subsequent decreases in nuclear p65 and p50 protein levels. Moreover, the phosphorylations of IKK, p38, ERK1/2, and JNK in LPS-stimulated RAW 264.7 cells were suppressed by Asiatic Acid in a dose-dependent manner. These results suggest that the anti-inflammatory properties of Asiatic Acid might be the results from the inhibition of iNOS, COX-2, IL-6, IL-1β, and TNF-α expressions through the down-regulation of NF-κB activation via suppression of IKK and MAP kinase (p38, ERK1/2, and JNK) phosphorylation in RAW 264.7 cells.
-
inhibition of lps induced no and pge2 production by Asiatic Acid via nf κb inactivation in raw 264 7 macrophages possible involvement of the ikk and mapk pathways
International Immunopharmacology, 2008Co-Authors: Kyungjin Yun, Hyunju Jung, Seo Young Jeong, Heejuhn Park, Jiyeon Kim, Jongbin Kim, Kyungwon Lee, Youngwuk Cho, Kijoo Yun, Kyungtae LeeAbstract:In the present study, we investigated the effect of Asiatic Acid (the aglycon of Asiaticoside) and Asiaticoside isolated from the leaves of Centella Asiatica (Umbelliferae) on LPS-induced NO and PGE(2) production in RAW 264.7 macrophage cells. Asiatic Acid more potently inhibited LPS-induced NO and PGE(2) production than Asiaticoside. Consistent with these observations, the protein and mRNA expression levels of inducible iNOS and COX-2 enzymes were inhibited by Asiatic Acid in a concentration-dependent manner. In addition, Asiatic Acid dose-dependently reduced the production of IL-6, IL-1 beta and TNF-alpha in LPS-stimulated RAW 264.7 macrophage cells. Furthermore, Asiatic Acid inhibited the NF-kappaB activation induced by LPS, and this was associated with the abrogation of I kappa B-alpha degradation and with subsequent decreases in nuclear p65 and p50 protein levels. Moreover, the phosphorylations of IKK, p38, ERK1/2, and JNK in LPS-stimulated RAW 264.7 cells were suppressed by Asiatic Acid in a dose-dependent manner. These results suggest that the anti-inflammatory properties of Asiatic Acid might be the results from the inhibition of iNOS, COX-2, IL-6, IL-1 beta, and TNF-alpha expressions through the down-regulation of NF-kappaB activation via suppression of IKK and MAP kinase (p38, ERK1/2, and JNK) phosphorylation in RAW 264.7 cells.
