Effect of Acupuncture on Muscle Endurance in the Female Shoulder Joint: A Pilot Study.

Shoulder joint dysfunction is the leading cause of decreased athletic ability in athletes. Shoulder joint sports injuries affect the athletic performance of athletes. Improvements in the muscle endurance of the shoulder joint can reduce the incidence of shoulder joint dysfunction. Acupuncture has been an important part of Asian culture for a long time. In acupuncture, nerves are stimulated, inducing postactivation potentiation (PAP) in the body's motor units and enhancing muscle strength. In this research, 20 female participants with full flexion/extension and adduction/abduction ranges of motion in the shoulder joint during isokinetic exercises underwent stimulation of the following acupuncture points in the shoulder joint: Binao (LI14), Jianyu (LI15), Jianliao (SJ14), Naohui (SJ13), Yuzhong (KI26), Zhongfu (LU1), Yunmen (LU2), Xiabai (LU4), Chize (LU5), Tianfu (LU3), and Xiaoluo (SJ12). In the study, there were significant increases after acupuncture in the average maximum torque in flexion, extension, and adduction; the average work in flexion/extension and adduction/abduction; the average power in flexion/extension and adduction/abduction; the total work in flexion/extension and adduction/abduction; the total net sagittal-plane work (flexion + extension); and the total net frontal-plane work (adduction + abduction) (P < 0.05). The average maximum abduction torque did not increase significantly, potentially due to antagonistic forces of muscles. Therefore, acupuncture at acupoints around the shoulder joint can increase muscle excitability, thereby delaying muscle fatigue and increasing muscle endurance.

Protective effects of TREK-1 against oxidative injury induced by SNP and H2O2.

AIM: TREK-1 (TWIK-related K+ channel-1) is a 2-pore-domain K+ channel subtype. The present study investigated the role of TREK-1 in cell death induced by oxidative stress. METHODS: The cell viability of wild-type Chinese hamster ovary (CHO) and TREK-1-transfected CHO cells (TREK-1/CHO cells) was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in the presence of sodium nitroprusside (SNP) or hydrogen peroxide (H2O2). Apoptosis of wild-type CHO and TREK-1/CHO cells was detected using Hoechst33342 staining. RESULTS: Both SNP and H2O2 caused dose- and time-dependent growth inhibition of wild-type CHO and TREK-1/ CHO cells. Following a 12 h exposure to SNP, the 50% inhibition (IC(50)) values for wild-type CHO and TREK-1/CHO cells were calculated as 0.69 mmol/L and 1.14 mmol/L, respectively. The IC(50) values were 0.07 mmol/L and 0.09 mmol/L in H2O2-treated wild-type CHO and TREK-1/CHO cells, respectively, following 12 h exposure to H2O2. Moreover, SNP/H2O2 induced less apoptosis in TREK-1/ CHO cells than that in wild-type CHO cells (P<0.05). CONCLUSION: The results demonstrated that TREK-1 played a protective role against oxidative injury.

Role of potassium channels in Abeta(1-40)-activated apoptotic pathway in cultured cortical neurons.

Potassium channel dysfunction has been implicated in Alzheimer's disease (AD). In the present study, by using potassium channel blocker tetraethylammonium (TEA), we investigated the relationship between the enhancement of potassium currents and the alteration of apoptotic cascade in the neuronal apoptotic model induced by beta-amyloid peptide 1-40(Abeta(1-40)). Cortical neurons exposed to Abeta(1-40) 5 muM developed a specific increase in the delayed rectifier potassium current (I(K)), but not the transient outward potassium currents (I(A)), before the appearance of neuronal apoptosis. Abeta(1-40) induced various apoptotic features such as chromatin condensation, a decrease in the amount of Bcl-2 protein, an increase in the amount of Bax protein, cytochrome c release from mitochondria, and caspase-3 activation. Potassium channel blocker 5 mM TEA attenuated Abeta(1-40)-induced neuronal death and prevented the alterations of all above mentioned apoptotic indicators. The study indicates that I(K) enhancement might play an important role in certain form of programmed cell death induced by beta-amyloid peptide (Abeta). Increased potassium channel activity might trigger the activation of apoptosis cascade in Abeta(1-40)-treated rat cortical neurons.

[mRNA expression of voltage-dependent potassium channels in the brain of rats after middle cerebral artery occlusion].

AIM: To study the mRNA expression changes in the brain of rats after middle cerebral artery occlusion. METHODS: Middle cerebral artery occlusion was used to induce ischemia in rat brain. The mRNA expression of voltage-dependent potassium channel subtypes, including Kv1.4, Kv1.5, Kv2.1 and Kv4.2, were detected in rat hippocampus and cortex by RT-PCR. RESULTS: Middle cerebral artery occlusion induced a significant neurological injury in rats. After ischemia 2 h, the mRNA of Kv1.4, Kv2.1 and Kv4.2 in hippocampus increased by 50%, 67% and 90% , respectively. And the mRNA of Kv1.4 and Kv4.2 maintained at a high level in hippocampus after ischemia 24 h. In cortex, the mRNA level of all the four subtypes were not changed significantly after ischemia 2 h, but the mRNA of Kv2.1 and Kv4.2 increased by 70% and 62% after ischemia 24 h, respectively. CONCLUSION: The mRNA expression levels of voltage-dependent potassium channels were up-regulated in rat hippocampus and cortex after middle cerebral artery occlusion.

Selective alteration of expression of Na+/Ca2+ exchanger isoforms after transient focal cerebral ischemia in rats.

The Na+/Ca2+ exchanger (NCX) is an antiporter located in the plasma membrane of many cells, which can maintain the intracellular Ca(2+) homeostasis. Some studies have shown the close relationship of NCX and cerebral ischemia. But controversial results were obtained. Three NCX isoforms, NCX1, NCX2, and NCX3 were distributed selectively in central nervous system, which suggests that each isoform may have different function in cerebral ischemia. In this study we investigated the time-related alteration of gene and protein expressions of NCX1, NCX2, and NCX3 in rat brain cortex after 2 h of transient middle cerebral artery occlusion (tMCAO). Reverse transcription-polymerase chain reaction (RT-PCR) was used to investigate the mRNA levels of each NCX isoform at 2, 6, 12, and 24 h of reperfusion, respectively. Western blot was used to measure the protein expressions of each NCX isoform at 2, 12, and 24 h of reperfusion, respectively. The results showed that NCX1 mRNA level was reduced by 42.1% and 27.8%, respectively, at 2 and 6h of reperfusion and restored to normal level at 12 and 24 h of reperfusion. NCX1 protein was decreased by 36.6% at 2 h of reperfusion and recovered at 12 and 24 h of reperfusion. The mRNA and protein levels of NCX2 and NCX3 did not change significantly over time. These results suggest that NCX1 might play an important role in transient focal cerebral ischemia.

Enhanced expressions of arachidonic acid-sensitive tandem-pore domain potassium channels in rat experimental acute cerebral ischemia.

To further explore the pathophysiological significance of arachidonic acid-sensitive potassium channels, RT-PCR and Western blot analysis were used to investigate the expression changes of TREK channels in cortex and hippocampus in rat experimental acute cerebral ischemia in this study. Results showed that TREK-1 and TRAAK mRNA in cortex, TREK-1 and TREK-2 mRNA in hippocampus showed significant increases 2 h after middle cerebral artery occlusion (MCAO). While the mRNA expression levels of the all three channel subtypes increased significantly 24 h after MCAO in cortex and hippocampus. At the same time, the protein expressions of all the three channel proteins showed significant increase 24 h after MCAO in cortex and hippocampus, but only TREK-1 showed increased expression 2 h after MCAO in cortex and hippocampus. Immunohistochemical experiments verified that all the three channel proteins had higher expression levels in cortical and hippocampal neurons 24 h after MCAO. These results suggested a strong correlation between TREK channels and acute cerebral ischemia. TREK channels might provide a neuroprotective mechanism in the pathological process.

Echinacoside rescues the SHSY5Y neuronal cells from TNFalpha-induced apoptosis.

We investigated the neuroprotective effect of echinacoside, one of the phenylethanoids isolated from the stems of Cistanches salsa, a Chinese herbal medicine, on tumor necrosis factor-alpha (TNFalpha)-induced apoptosis in human neuroblastoma (SHSY5Y) cells. Treatment of cultured SHSY5Y cells with TNFalpha 100 ng ml(-1) for 36 h stimulated apoptosis, as demonstrated by typical morphological changes, cell viability, DNA laddering, annexin-V binding, intracellular reactive oxygen species, mitochondrial membrane potential and caspase-3 activity. However, simultaneous treatment with echinacoside (1, 10 or 100 microg ml(-1)) attenuated the TNFalpha-mediated apoptosis. The antiapoptotic action of echinacoside was partially dependent on antioxidative stress effects, maintenance of mitochondria function, inhibition of caspase-3 activity and was also associated with increasing the expression of the antiapoptotic protein Bcl2. Thus, echinacoside has the neuroprotective capacity to antagonize TNFalpha-induced apoptosis in SHSY5Y cells and may be useful in treating some neurodegenerative diseases.

Protective effect of tubuloside B on TNFalpha-induced apoptosis in neuronal cells.

AIM: To investigate the neuroprotective effect of tubuloside B, one of the phenylethanoids isolated from the stems of Cistanche salsa, on tumor necrosis factor-alpha (TNFalpha)-induced apoptosis in SH-SY5Y neuronal cells. METHODS: Cell viability was analyzed using MTT assay. Apoptotic cells were detected using Hoechst33342 staining, and confirmed by DNA fragmentation and flow cytometric analysis. The activity of caspase-3 was measured with special assay kit. The concentration of free intracellular calcium was determined with the probe Indo-1 by spectrometer. The level of intracellular reactive oxygen species and the potential of mitochondrial membrane were determined by laser scanning confocal microscopy (LSCM) combined with fluorescence probe H2DCFDA or JC-1 respectively. RESULTS: SH-SY5Y cells treated with TNFalpha 100 microg/L for 36 h showed typical morphological changes of apoptosis. DNA ladder could be observed by agarose gel electrophoresis. The highest percentage of apoptotic cells accumulated to 37.5 %. Following 36 h treatment with TNFalpha, accumulation of intracellular ROS and [Ca2+]i and decrease in mitochondrial membrane potential were observed, and caspase-3 activity increased by about five-fold compared with controls. However, pretreatment with tubuloside B (1, 10, or 100 mg/L) for 2 h attenuated the TNFalpha-mediated apoptosis. The antiapoptotic action of tubuloside B was partially dependent on an anti-oxidative stress effects, maintain of mitochondria function, decrease of concentration of free intracellular calcium and inhibition of caspase-3 activity. CONCLUSION: Tubuloside B has the neuroprotective capacity to antagonize TNFalpha-induced apoptosis in SH-SY5Y cells and may be useful in treating some neurodegenerative diseases.