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Gu Q.,Shanghai Research Center for Acupuncture and Meridians | Gu Q.,Shanghai University of Traditional Chinese Medicine | Wang L.,Shanghai Research Center for Acupuncture and Meridians | Huang F.,Fudan University | And 2 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2012

Low-level laser irradiation of visible light had been introduced as a medical treatment already more than 40 years ago, but its medical application still remains controversial. Laser stimulation of acupuncture points has also been introduced, and mast-cells degranulation has been suggested. Activation of TRPV ion channels may be involved in the degranulation. Here, we investigated whether TRPV1 could serve as candidate for laser-induced mast cell activation. Activation of TRPV1 by capsaicin resulted in degranulation. To investigate the effect of laser irradiation on TRPV1, we used the Xenopus oocyte as expression and model system. We show that TRPV1 can functionally be expressed in the oocyte by (a) activation by capsaicin (K1/2 = 1.1 M), (b) activation by temperatures exceeding 42°C, (c) activation by reduced pH (from 7.4 to 6.2), and (d) inhibition by ruthenium red. Red (637 nm) as well as blue (406 nm) light neither affected membrane currents in oocytes nor did it modulate capsaicin-induced current. In contrast, green laser light (532 nm) produced power-dependent activation of TRPV1. In conclusion, we could show that green light is effective at the cellular level to activate TRPV1. To which extend green light is of medical relevance needs further investigation. © 2012 Quanbao Gu et al. Source

Lundberg Y.W.,Boys Town National Research Hospital | Xu Y.,Boys Town National Research Hospital | Xu Y.,Shanghai Research Center for Acupuncture and Meridians | Thiessen K.D.,Creighton University | Kramer K.L.,Creighton University
Developmental Dynamics | Year: 2015

Otoconia are bio-crystals that couple mechanic forces to the sensory hair cells in the utricle and saccule, a process essential for us to sense linear acceleration and gravity for the purpose of maintaining bodily balance. In fish, structurally similar bio-crystals called otoliths mediate both balance and hearing. Otoconia abnormalities are common and can cause vertigo and imbalance in humans. However, the molecular etiology of these illnesses is unknown, as investigators have only begun to identify genes important for otoconia formation in recent years. Results: To date, in-depth studies of selected mouse otoconial proteins have been performed, and about 75 zebrafish genes have been identified to be important for otolith development. Conclusions: This review will summarize recent findings as well as compare otoconia and otolith development. It will provide an updated brief review of otoconial proteins along with an overview of the cells and cellular processes involved. While continued efforts are needed to thoroughly understand the molecular mechanisms underlying otoconia and otolith development, it is clear that the process involves a series of temporally and spatially specific events that are tightly coordinated by numerous proteins. Such knowledge will serve as the foundation to uncover the molecular causes of human otoconia-related disorders. © 2014 Wiley Periodicals, Inc. Source

Zhou F.,Shanghai Research Center for Acupuncture and Meridians | Guo J.,Fudan University | Cheng J.,Fudan University | Wu G.,Fudan University | And 3 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2013

Electroacupuncture (EA) has been shown to increase cerebral blood flow (CBF) and reduce ischemic infarction in the rat model of cerebral ischemia (middle cerebral artery occlusion, MCAO). Since multiple acupoints are recommended to treat cerebral ischemia, we performed this study to investigate if there is any variation in EA protection against cerebral ischemia with the stimulation of certain "acupoints" in rats. One hour of right MCAO with an 85% reduction of blood flow induced an extensive infarction (32.9% ± 3.8% of the brain), serious neurological deficits (scale = 6.0 ± 0.5, on a scale of 0-7), and a 17% (10 out of 60) mortality. EA, with a sparse-dense wave (5 Hz/20 Hz) at 1.0 mA for 30 minutes, at Du 20 and Du 26 greatly reduced the infarction to 4.5% ± 1.5% (P<0.01), significantly improved neurological deficit (scale = 1.0 ± 0.5, P<0.01), and decreased the death rate to 7% (2 out of 30, P<0.01). Similarly, EA at left LI 11 & PC 6 reduced the infarct volume to 8.6% ± 3.8% (P<0.01), improved the neurological deficit (scale = 2.0 ± 1.0, P<0.01), and decreased the death rate to 8% (2 out of 24, P<0.01). In sharp contrast, EA at right LI 11 & PC 6 did not lead to any significant changes in the infarct volume (33.4% ± 6.3%), neurological deficit (scale = 6.5 ± 0.5), and the death rate (20%, 5 out of 24). EA at left GB 34 & SP 6, also had an inconspicuous effect on the ischemic injury. EA at Du 20 & Du 26 or at left LI 11 & PC 6 instantaneously induced a significant increase in cerebral blood flow. Neither EA at right LI 11 & PC 6 nor at GB 34 & SP 6 increased cerebral blood flow. These results revealed that the EA protection against cerebral ischemia is relatively acupoint specific. © 2013 Fei Zhou et al. Source

Tian X.,Fudan University | Tian X.,University of Houston | Guo J.,Fudan University | Guo J.,Shanghai Research Center for Acupuncture and Meridians | And 4 more authors.
PLoS ONE | Year: 2013

Objectives:δ-opioid receptor (DOR) activation reduced brain ischemic infarction and attenuated neurological deficits, while DOR inhibition aggravated the ischemic damage. The underlying mechanisms are, however, not well understood yet. In this work, we asked if DOR activation protects the brain against ischemic injury through a brain-derived neurotrophic factor (BDNF) -TrkB pathway.Methods:We exposed adult male Sprague-Dawley rats to focal cerebral ischemia, which was induced by middle cerebral artery occlusion (MCAO). DOR agonist TAN-67 (60 nmol), antagonist Naltrindole (100 nmol) or artificial cerebral spinal fluid was injected into the lateral cerebroventricle 30 min before MCAO. Besides the detection of ischemic injury, the expression of BDNF, full-length and truncated TrkB, total CREB, p-CREB, p-ATF and CD11b was detected by Western blot and fluorescence immunostaining.Results:DOR activation with TAN-67 significantly reduced the ischemic volume and largely reversed the decrease in full-length TrkB protein expression in the ischemic cortex and striatum without any appreciable change in cerebral blood flow, while the DOR antagonist Naltrindole aggregated the ischemic injury. However, the level of BDNF remained unchanged in the cortex, striatum and hippocampus at 24 hours after MCAO and did not change in response to DOR activation or inhibition. MCAO decreased both total CREB and pCREB in the striatum, but not in the cortex, while DOR inhibition promoted a further decrease in total and phosphorylated CREB in the striatum and decreased pATF-1 expression in the cortex. In addition, MCAO increased C11b expression in the cortex, striatum and hippocampus, and DOR activation specifically attenuated the ischemic increase in the cortex but not in the striatum and hippocampus.Conclusions:DOR activation rescues TrkB signaling by reversing ischemia/reperfusion induced decrease in the full-length TrkB receptor and reduces brain injury in ischemia/reperfusion. © 2013 Tian et al. Source

Zhou F.,Shanghai Research Center for Acupuncture and Meridians | Guo J.,Fudan University | Cheng J.,Fudan University | Wu G.,Fudan University | And 2 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2013

We explored the optimal duration of electroacupuncture (EA) stimulation for protecting the brain against ischemic injury. The experiments were carried out in rats exposed to right middle cerebral artery occlusion (MCAO) for 60 min followed by 24-hr reperfusion. EA was delivered to "Shuigou" (Du 26) and "Baihui" (Du 20) acupoints with sparse-dense wave (5/20 Hz) at 1.0 mA for 5, 15, 30, and 45 min, respectively. The results showed that 30 min EA, starting at 5 minutes after the onset of MCAO (EA during MCAO) or 5 minutes after reperfusion (EA after MCAO), significantly reduced ischemic infarct volume, attenuated neurological deficits, and decreased death rate with a larger reduction of the ischemic infarction in the former group. Also in the group of EA during MCAO, this protective benefit was positively proportional to the increase in the period of stimulation, that is, increased protection in response to EA from 5- to 30-min stimulation. In all groups, EA induced a significant increase in cerebral blood flow and promoted blood flow recovery after reperfusion, and both blood flow volume and blood cell velocity returned to the preischemia level in a short period of time. Surprisingly, EA for 45 min did not show reduction in the neurological deficits or the infarct volume and instead demonstrated an increase in death rate in this group. Although EA for 45 min still increased the blood flow during MCAO, it led to a worsening of perfusion after reperfusion compared to the group subjected only to ischemia. The neuroprotection induced by an "optimal" period (30 min) of EA was completely blocked by Naltrindole, a δ-opioid receptor (DOR) antagonist (10 mg/kg, i.v.). These findings suggest that earlier EA stimulation leads to better outcomes, and that EA-induced neuroprotection against ischemia depends on an optimal EA-duration via multiple pathways including DOR signaling, while "over-length" stimulation exacerbates the ischemic injury. © 2013 Fei Zhou et al. Source

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