5 results on '"Cheng, Elaine"'
Search Results
2. Neuroprotective effect of a novel Chinese herbal decoction on cultured neurons and cerebral ischemic rats.
- Author
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Chui-Fun Ip, Fanny, Yu-Ming Zhao, Kim-Wan Chan, Yee-Ling Cheng, Elaine, Pui-Sze Tong, Estella, Chandrashekar, Oormila, Guang-Miao Fu, Zhong-Zhen Zhao, and Yuk-Yu Ip, Nancy
- Subjects
ANALYSIS of variance ,ANIMAL experimentation ,DOSE-effect relationship in pharmacology ,ELECTROPHYSIOLOGY ,HERBAL medicine ,HIGH performance liquid chromatography ,IMMUNOHISTOCHEMISTRY ,CHINESE medicine ,RATS ,RESEARCH funding ,STATISTICS ,T-test (Statistics) ,WESTERN immunoblotting ,DATA analysis ,NEUROPROTECTIVE agents ,STROKE rehabilitation ,DESCRIPTIVE statistics ,IN vitro studies ,IN vivo studies ,PHARMACOKINETICS - Abstract
Background: Historically, traditional Chinese medicine has been widely used to treat stroke. Based on the theory of Chinese medicine and the modern pharmacological knowledge of herbal medicines, we have designed a neuroprotective formula called Post-Stroke Rehabilitation (PSR), comprising seven herbs -- Astragalus membranaceus (Fisch.) Bunge, Salvia miltiorrhiza Bunge, Paeonia lactiflora Pall., Cassia obtusifolia L., Ligusticum chuanxiong Hort., Angelica sinensis (Oliv.) Diels, and Glycyrrhiza uralensis Fisch. We aim to examine the neuroprotective activity of PSR in vitro and in vivo, and to explore the underlying molecular mechanisms, to better understand its therapeutic effect and to further optimize its efficacy. Methods: PSR extract or vehicle was applied to primary rat neurons to examine their survival effects against N- methyl-D-aspartate (NMDA)-elicited excitotoxicity. Whole-cell patch-clamp recording was conducted to examine the NMDA-induced current in the presence of PSR. ERK- and CREB-activation were revealed by western blot analysis. Furthermore, PSR was tested for CRE promoter activation in neurons transfected with a luciferase reporter. The protective effect of PSR was then studied in the rat middle cerebral artery occlusion (MCAO) model. MCAO rats were either treated with PSR extract or vehicle, and their neurobehavioral deficit and cerebral infarct were evaluated. Statistical differences were analyzed by ANOVA or t-test. Results: PSR prominently reduced the death of cultured neurons caused by NMDA excitotoxicity in a dose-dependent manner, indicating its neuroprotective property. Furthermore, PSR significantly reduced NMDA-evoked current reversibly and activated phosphorylation of ERK and CREB with distinct time courses, with the latter's kinetics slower. PSR also triggered CRE-promoter activity as revealed by the increased expression of luciferase reporter in transfected neurons. PSR effectively reduced cerebral infarct and deficit in neurological behavior in MCAO rats when PSR decoction was administered starting either 6 days before or 6 h after onset of ischemia. Conclusions: PSR is neuroprotective both in vitro and in vivo -- it protects cultured neurons against NMDA excitotoxicity, and effectively reduces ischemic injury and neurobehavioral deficit in MCAO rats in both the pre- and post-treatment regimens. The underlying neuroprotective mechanisms may involve inhibition of NMDA receptor current and activation of ERK and CREB. This study provides important preclinical data necessary for the further development of PSR for stroke treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
3. Incidence of the V600K mutation amongmelanoma patients with BRAF mutations, andpotential therapeutic response to the specificBRAF inhibitor PLX4032.
- Author
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Rubinstein, Jill C., Sznol, Mario, Pavlick, Anna C., Ariyan, Stephan, Cheng, Elaine, Bacchiocchi, Antonella, Kluger, Harriet M., Narayan, Deepak, and Halaban, Ruth
- Subjects
MELANOMA ,CANCER treatment ,CLINICAL trials ,GENETIC mutation ,LETHAL mutations ,PATIENTS - Abstract
Activating mutations in BRAF kinase are common in melanomas. Clinical trials with PLX4032, the mutant-BRAF inhibitor, show promising preliminary results in patients selected for the presence of V600E mutation. However, activating V600K mutation is the other most common mutation, yet patients with this variant are currently excluded from the PLX4032 trials. Here we present evidence that a patient bearing the BRAF V600K mutation responded remarkably to PLX4032, suggesting that clinical trials should include all patients with activating BRAF V600E/K mutations. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
- View/download PDF
4. Neuroprotective effect of a novel Chinese herbal decoction on cultured neurons and cerebral ischemic rats.
- Author
-
Ip FC, Zhao YM, Chan KW, Cheng EY, Tong EP, Chandrashekar O, Fu GM, Zhao ZZ, and Ip NY
- Subjects
- Animals, Brain Ischemia pathology, Cells, Cultured, Drugs, Chinese Herbal chemistry, Infarction, Middle Cerebral Artery metabolism, Male, Neurons cytology, Neuroprotective Agents chemistry, Rats, Rats, Sprague-Dawley, Signal Transduction, Brain Ischemia metabolism, Drugs, Chinese Herbal pharmacology, Neurons drug effects, Neuroprotective Agents pharmacology
- Abstract
Background: Historically, traditional Chinese medicine has been widely used to treat stroke. Based on the theory of Chinese medicine and the modern pharmacological knowledge of herbal medicines, we have designed a neuroprotective formula called Post-Stroke Rehabilitation (PSR), comprising seven herbs - Astragalus membranaceus (Fisch.) Bunge, Salvia miltiorrhiza Bunge, Paeonia lactiflora Pall., Cassia obtusifolia L., Ligusticum chuanxiong Hort., Angelica sinensis (Oliv.) Diels, and Glycyrrhiza uralensis Fisch. We aim to examine the neuroprotective activity of PSR in vitro and in vivo, and to explore the underlying molecular mechanisms, to better understand its therapeutic effect and to further optimize its efficacy., Methods: PSR extract or vehicle was applied to primary rat neurons to examine their survival effects against N-methyl-D-aspartate (NMDA)-elicited excitotoxicity. Whole-cell patch-clamp recording was conducted to examine the NMDA-induced current in the presence of PSR. ERK- and CREB-activation were revealed by western blot analysis. Furthermore, PSR was tested for CRE promoter activation in neurons transfected with a luciferase reporter. The protective effect of PSR was then studied in the rat middle cerebral artery occlusion (MCAO) model. MCAO rats were either treated with PSR extract or vehicle, and their neurobehavioral deficit and cerebral infarct were evaluated. Statistical differences were analyzed by ANOVA or t-test., Results: PSR prominently reduced the death of cultured neurons caused by NMDA excitotoxicity in a dose-dependent manner, indicating its neuroprotective property. Furthermore, PSR significantly reduced NMDA-evoked current reversibly and activated phosphorylation of ERK and CREB with distinct time courses, with the latter's kinetics slower. PSR also triggered CRE-promoter activity as revealed by the increased expression of luciferase reporter in transfected neurons. PSR effectively reduced cerebral infarct and deficit in neurological behavior in MCAO rats when PSR decoction was administered starting either 6 days before or 6 h after onset of ischemia., Conclusions: PSR is neuroprotective both in vitro and in vivo - it protects cultured neurons against NMDA excitotoxicity, and effectively reduces ischemic injury and neurobehavioral deficit in MCAO rats in both the pre- and post-treatment regimens. The underlying neuroprotective mechanisms may involve inhibition of NMDA receptor current and activation of ERK and CREB. This study provides important preclinical data necessary for the further development of PSR for stroke treatment.
- Published
- 2016
- Full Text
- View/download PDF
5. Incidence of the V600K mutation among melanoma patients with BRAF mutations, and potential therapeutic response to the specific BRAF inhibitor PLX4032.
- Author
-
Rubinstein JC, Sznol M, Pavlick AC, Ariyan S, Cheng E, Bacchiocchi A, Kluger HM, Narayan D, and Halaban R
- Subjects
- Amino Acid Substitution genetics, Base Sequence, DNA Mutational Analysis, Humans, Melanoma enzymology, Molecular Sequence Data, Protein Kinase Inhibitors therapeutic use, Skin Neoplasms enzymology, Vemurafenib, Indoles therapeutic use, Melanoma drug therapy, Melanoma genetics, Mutation genetics, Proto-Oncogene Proteins B-raf genetics, Skin Neoplasms drug therapy, Skin Neoplasms genetics, Sulfonamides therapeutic use
- Abstract
Activating mutations in BRAF kinase are common in melanomas. Clinical trials with PLX4032, the mutant-BRAF inhibitor, show promising preliminary results in patients selected for the presence of V600E mutation. However, activating V600K mutation is the other most common mutation, yet patients with this variant are currently excluded from the PLX4032 trials. Here we present evidence that a patient bearing the BRAF V600K mutation responded remarkably to PLX4032, suggesting that clinical trials should include all patients with activating BRAF V600E/K mutations.
- Published
- 2010
- Full Text
- View/download PDF
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