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Points - Recent Research
Acupuncture Stimulation of Taichong (Liv3) and Hegu (LI4) Modulates the Default Mode Network Activity in Alzheimer's Disease
Therapeutic Effect and Mechanism of Electroacupuncture at Zusanli on Plasticity of Interstitial Cells of Cajal
Ginsenosides Attenuate Methylglyoxal-Induced Impairment of Insulin Signaling and Subsequent Apoptosis in Primary Astrocytes

Acupuncture Stimulation of Taichong (Liv3) and Hegu (LI4) Modulates the Default Mode Network Activity in Alzheimer's Disease

Liang P1, et al.

OBJECTIVES: The acupuncture has been used in the therapy of Alzheimer disease (AD), however, its neural underpins are still unclear. The aim of this study is to examine the acupuncture effect on the default mode network (DMN) in AD by using resting state functional magnetic resonance imaging (RS-fMRI). METHODS: Twenty-eight subjects (14 AD and 14 normal controls (NC)) participated in this study. RS-fMRI data were acquired before and after acupuncture, while during the acupuncture, the procession of acupuncture stimulation on the acupoints of Tai chong (Liv3) and Hegu (LI4) lasted for 3 minutes. RESULTS: Region of interest analysis showed that the impaired DMN connectivity in AD (identified by comparing the pre-acupuncture RS-fMRI of AD and NC), specifically the left cingulate gyrus (CG) and right inferior parietal lobule (IPL), were significantly changed for the better. The whole-brain exploratory analysis further demonstrated these results and found some new regions respond to the acupuncture effect on AD, with a cluster in the left posterior cingulate cortex (PCC), the right middle temporal gyrus (MTG) together with right IPL showed increased within-DMN connectivity; and the bilateral CG and left PCu showed decreased within-DMN connectivity. Moreover, the acupuncture effect on the right MTG was significantly correlated with disease severity as measured by Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores. CONCLUSION: It was found that the acupuncture stimulation could modulate the DMN activity in AD. The current findings suggest that the acupuncture treatment on the relative earlier AD patients might have a better therapy effect.

Am J Alzheimers Dis Other Demen. 2014 Jun 6. pii: 1533317514536600. [Epub ahead of print]

Source: PubMed

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Therapeutic Effect and Mechanism of Electroacupuncture at Zusanli on Plasticity of Interstitial Cells of Cajal

Peng MF, et al.

BACKGROUND: Electroacupuncture (EA) is one of the techniques of acupuncture and is believed to be an effective alternative and complementary treatment in many disorders. The aims of this study were to investigate the effects and mechanisms of EA at acupoint Zusanli (ST36) on the plasticity of interstitial cells of Cajal (ICCs) in partial bowel obstruction. METHODS: A Sprague Dawley rat model of partial bowel obstruction was established and EA was conducted at Zusanli (ST36) and Yinglingquan (SP9) in test and control groups, respectively. Experiments were performed to study the effects and mechanisms of EA at Zusanli on intestinal myoelectric activity, distribution and alteration of ICCs, expression of inflammatory mediators, and c-Kit expression. RESULTS: 1) EA at Zusanli somewhat improved slow wave amplitude and frequency in the partial obstruction rats. 2) EA at Zusanli significantly stimulated the recovery of ICC networks and numbers. 3) the pro-inflammatory mediator TNF-alpha and NO activity were significantly reduced after EA at Zusanli, However, no significant changes were observed in the anti-inflammatory mediator IL-10 activity. 4) EA at Zusanli re-expressed c-Kit protein. However, EA at the control acupoint, SP9, significantly improved slow wave frequency and amplitude, but had no effect on ICC or inflammatory mediators. CONCLUSIONS: We concluded that EA at Zusanli might have a therapeutic effect on ICC plasticity, and that this effect might be mediated via a decrease in pro-inflammatory mediators and through the c-Kit signaling pathway, but that the relationship between EA at different acupoints and myoelectric activity needs further study.

BMC Complement Altern Med.2014 Jun 7;14(1):186. [Epub ahead of print]

Source: PubMed

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Ginsenosides Attenuate Methylglyoxal-Induced Impairment of Insulin Signaling and Subsequent Apoptosis in Primary Astrocytes

Chu JM1, et al.

Diabetes mellitus (DM), which is characterized by chronic hyperglycemia, is known to increase the risk of neurodegeneration. In type 2 diabetes, hyperglycemia could cause insulin resistance and neurodegeneration in various cells including neurons and astrocytes. Hyperglycemia is also known to result in the formation of advanced glycation end-products (AGE) Methylglyoxal (MG) is one of the most reactive AGE precursors in which its abnormal accumulation is usually found in diabetic patients and induces neuronal cell death in central nervous system. Ginseng is a herb that has been widely used to treat various diseases in traditional Chinese medicine. Ginsenosides, the pharmacologically active component isolated from ginseng, have been shown to have cryoprotective effects in different neural cells. In the present study we investigated the effects of MG in disturbing insulin signaling and leading to further cellular apoptosis in rat primary astrocytes. Furthermore, the protective effects of different subtypes of ginsenosides were studied. From the results, impairment of insulin signaling was found in astrocytes under MG treatment. Moreover, cleavage of caspase and Poly ADP ribose polymerase (PARP) was observed in line with insulin signaling disruption, showing the neurotoxic effects of MG towards astrocytes. The effects of ginsenosides in MG treated astrocytes were also investigated. After treatment, ginsenosides Rd and R-Rh2 were shown to ameliorate the cell viability of MG-treated astrocytes. In addition, Rd and R-Rh2 could improve insulin signaling and inhibit apoptosis, indicating that Rd, R-Rh2 and related compounds may have therapeutic potential in treating diabetes-induced neurodegeneration.

Neuropharmacology. 2014 May 28;85C:215-223. doi: 10.1016/j.neuropharm.2014.05.029. [Epub ahead of print]

Source: PubMed

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