Points - Recent Research
Electroacupuncture Acutely Improves Cerebral Blood Flow and Attenuates Moderate Ischemic Injury via an Endothelial Mechanism in Mice
Ganoderma Lucidum Ethanol Extract Inhibits the Inflammatory Response in Lipopolysaccharide (LPS)-Stimulated Murine BV2 Microglia
In Vitro Anti-Proliferative Effects of Zuojinwan on Eight Kinds of Human Cancer Cell Lines

Electroacupuncture Acutely Improves Cerebral Blood Flow and Attenuates Moderate Ischemic Injury via an Endothelial Mechanism in Mice

Kim JH, et al. Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam, Republic of Korea.

Electroacupuncture (EA) is a novel therapy based on traditional acupuncture combined with modern eletrotherapy that is currently being investigated as a treatment for acute ischemic stroke. Here, we studied whether acute EA stimulation improves tissue and functional outcome following experimentally induced cerebral ischemia in mice. We hypothesized that endothelial nitric oxide synthase (eNOS)-mediated perfusion augmentation was related to the beneficial effects of EA by interventions in acute ischemic injury. EA stimulation at Baihui (GV20) and Dazhui (GV14) increased cerebral perfusion in the cerebral cortex, which was suppressed in eNOS KO, but there was no mean arterial blood pressure (MABP) response. The increased perfusion elicited by EA were completely abolished by a muscarinic acetylcholine receptor (mAChR) blocker (atropine), but not a β-adrenergic receptor blocker (propranolol), an α-adrenergic receptor blocker (phentolamine), or a nicotinic acetylcholine receptor (nAChR) blocker (mecamylamine). In addition, EA increased acetylcholine (ACh) release and mAChR M3 expression in the cerebral cortex. Acute EA stimulation after occlusion significantly reduced infarct volume by 34.5% when compared to a control group of mice at 24 h after 60 min-middle cerebral artery occlusion (MCAO) (moderate ischemic injury), but not 90-min MCAO (severe ischemic injury). Furthermore, the impact of EA on moderate ischemic injury was totally abolished in eNOS KO. Consistent with a smaller infarct size, acute EA stimulation led to prominent improvement of neurological function and vestibule-motor function. Our results suggest that acute EA stimulation after moderate focal cerebral ischemia, but not severe ischemia improves tissue and functional recovery and ACh/eNOS-mediated perfusion augmentation might be related to these beneficial effects of EA by interventions in acute ischemic injury.

PLoS One.2013;8(2):e56736. Epub 2013 Feb 13.

Source: PubMed

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Ganoderma Lucidum Ethanol Extract Inhibits the Inflammatory Response in Lipopolysaccharide (LPS)-Stimulated Murine BV2 Microglia

Yoon HM, et al. Departments of Acupuncture and Moxibustion, Dongeui University College of Oriental Medicine, Busan 614-052;

Ganoderma lucidum is a traditional Oriental medicine that has been widely used as a tonic to promote longevity and health in Korea and other Asian countries. Although a great deal of work has been carried out on the therapeutic potential of this mushroom, the pharmacological mechanisms of its anti-inflammatory actions remain unclear. In this study, we evaluated the inhibitory effects of G. lucidum ethanol extract (EGL) on the production of inflammatory mediators and cytokines in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. We also investigated the effects of EGL on the LPS-induced activation of nuclear factor kappaB (NF-κB) and upregulation of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). Elevated levels of nitric oxide (NO), prostaglandin E(2) (PGE(2)) and pro-inflammatory cytokine production were detected in BV2 microglia following LPS stimulation. We identifed that EGL significantly inhibits the excessive production of NO, PGE(2) and pro-inflammatory cytokines, including interleukin (IL)-1β and tumor necrosis factor-α in a concentration-dependent manner without causing cytotoxicity. In addition, EGL suppressed NF-κB translocation and transcriptional activity by blocking IκB degradation and inhibiting TLR4 and MyD88 expression in LPS-stimulated BV2 cells. Our results indicate that the inhibitory effects of EGL on LPS-stimulated inflammatory responses in BV2 microglia are associated with the suppression of the NF-κB and TLR signaling pathways. Therefore, EGL may be useful in the treatment of neurodegenerative diseases by inhibiting inflammatory mediator responses in activated microglia.

Exp Ther Med.2013 Mar;5(3):957-963. Epub 2013 Jan 15.

Source: PubMed

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In Vitro Anti-Proliferative Effects of Zuojinwan on Eight Kinds of Human Cancer Cell Lines

Xu L, et al. College of Pharmacy, Dalian Medical University, 9 Western Lvshun South Road, Dalian, 116044, China.

Zuojinwan (ZJW), a famous Chinese medicinal formula, contains two medicinal herbs Coptis chinese Frach and Evodia rutaecarpa (Juss.) Benth in the ratio of 6: 1. The inhibitory effects of ZJW on eight kinds of human cancer cell lines including SMMC-7721, BEL-7402, BEL-7404, HepG2, A549, NCI-H446, NCI-H460 and HCT- 116 cells were evaluated, and the possible mechanism was investigated. The growths of the eight kinds of cancer cells were inhibited by ZJW assessed through MTT assay. Flow cytometry assay revealed a sub-G1 peak with reduced DNA content was formed. The cell cycle was arrested in the G0/G1 phase in ZJW-treated SMMC-7721 and HepG2 cells, and in the S phase for NCI-H460 cells. Significant DNA damage was produced by ZJW assessed with single-cell gel electrophoresis assay. Morphological changes were also observed. Caspase-3 and -9 activities were increased following ZJW treatment. Western blot analysis showed that Bax and Bak protein levels were increased after ZJW treatment, while Bcl-2 and Bcl-xl protein levels were decreased. Our results suggest that ZJW has significant anti-cancer activities due to induction of mitochondria- dependent apoptosis pathway. Therefore, ZJW has the potential to be a novel chemotherapy drug to treat hepatoma, lung cancer and colon cancer by suppressing tumor growth.

Cytotechnology.2013 Feb 9. [Epub ahead of print]

Source: PubMed

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