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Aim To investigate the effect of chronic intermittent hypobaric hypoxia ( CIHH) on the paeonol induced vasomotion of isolated rat ’ s thoracic aorta rings and its underlying mechanisms. Methods Spra-gue-Dawlay ( SD ) rats were randomly divided into 2 groups: control group ( CON ) and CIHH treatment group ( CIHH) . CIHH rats were exposed to hypoxia in a hypobaric chamber simulating 5 000 m altitude, 6 hours daily for 28 days. CON rats lived in the same en-vironment as CIHH animals except hypoxia. Organ bath technique was used to observe the effect of pae-onol on isolated thoracic aorta rings of rats. Results There were no significant differences of noradrenaline ( NE )- and KCl-induced contraction in thoracic aorta rings among CIHH and CON rats;CIHH enhanced va-sodilative effects of paeonol on isolated thoracic aorta rings of rats; the vasodilative effects on CIHH rats could be partly decreased by β-receptor blocker prop-ranolol,ATP-sensitive potassium channel ( KATP ) bloc-ker glibenclamide and NO synthase inhibitor L-NAME. Paeonol significantly inhibited NE-induced intracellular and extracellular calcium-dependent contraction in CIHH rats. Paeonol didn ’ t inhibit NE-induced con-traction by intracellular calcium release and its inhibi-tory effect couldn ’ t be blocked by glibenclamide in CON. Vasodilative effects of paeonol couldn ’ t be re-versed by indomethacin, a cyclooxygenase inhibitor, in CIHH and CON rats. Conclusion CIHH significantly enhances vasodilative effects of paeonol on isolated tho-racic aorta rings of rats. Besides promoting the signa-ling pathway of paeonol in CON, CIHH significantly enhances vasodilative effects of paeonol via activating KATP and inhibiting Ca2+ release from sarcoplasmic re-ticulum.
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Aim To observe the cardioprotection of chronic intermittent hypobaric hypoxia (CIHH) against ischemia/reperfusion injury in adult and young rats.Methods Adult and postnatal male Sprague-Dawley rats were divided randomly into four groups:control 28-day group (CON28),control 42-day group (CON42), CIHH 28-day treatment group (CIHH28), and CIHH 42-day treatment group (CIHH42). CIHH animals with maternal rats were put into a hypobaric chamber 2 days before birth to get 28 days and 42 days CIHH mimicking 3000 m altitude (P_B=525 mmHg,P_(O_2)=108.8 mmHg), 5 h daily, respectively.The control animals were kept in the same environment as CIHH rats with free access to water and food except hypoxic exposure. The isolated hearts were perfused in the Langendorff apparatus, undergoing 30 min global ischemia and 60 min reperfusion.Cardiac function was recorded continuously during the whole experiment. Parameters of left ventricular function included left ventricular developing pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), maximal positive (+LVdp/dt) and negative (-LVdp/dt) velocity of left ventricular pressure, coronary flow (CF) and heart rate(HR).Results ① For adult rats, there was no significant difference in the parameters of left ventricular function between CIHH28 and CON28 groups. However, the recovery of cardiac function in CIHH42 rats was much better than that in CON42, including LVDP, LVEDP, ±LVdp/dt and CF (P<0.05). ② For young rats, the basic coronary flow (CF) in CIHH rats was significant higher than that in CON rats, while other parameters of cardiac function didn't change. The recovery of cardiac function in CIHH rats was much better than that in CON rats, including LVDP, LVEDP,±LVdp/dt and CF (P<0.05).Conclusion CIHH confers cardioprotection against ischemia/reperfusion injury in rat cardiomyocytes, which is predominant in CIHH42 group and significantly affected by the age of animals. Cardioprotective effects produce more easily in young rats by CIHH.
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Aim To investigate the effect of ginsenoside Rg1 on gut injury following intestinal ischemia reperfusion in rats and the possible mechanism.Methods By using rat model of intestinal I/R injury, 30 male SD rats were randomly divided into 3 groups(n =10 in each group):sham-operation group, I/R group(control group)and ginsenoside Rg1 group(treatment group).The contents of tumor necrosis factor α(TNF-α), interleukin-6(IL-6), malondialdehyde(MDA), the activity of superoxide dismutase(SOD)in intestinal mucosa were measured respectively.Chiu's count was used to assess the changes in intestinal pathological morphology.Results TNF-α, IL-6, MDA contents and the intestinal injury score in control group were significantly increased compared to those in sham-operation group, while SOD contents in control group were significantly decreased compared to sham-operation group.Inversely, TNF-α, IL-6, MDA contents and the intestinal injury score in treatment group were significantly decreased compared to those in control group, while SOD contents in treatment group were significantly increased compared to control group.Conclusion Pretreatment with ginsenoside Rg1 has protective effect on intestinal ischemia-reperfusion injury in rats, which may be attributed to decreased contents of TNF-α, IL-6, MDA and increased levels of SOD.
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Aim To observe the influences of ginsenoside Rg1 on the spontaneous contraction of small intestine smooth muscle of rabbits in vitro and explore the mechanism.Methods With the isothermal perfusion of small intestine in vitro,the influences of ginsenoside Rg1 on the spontaneous contraction of small intestine was observed and the mechanism of ginsenoside Rg1 was studied.Results Ginsenoside Rg1 reduced the amplitude of contraction of small intestine smooth muscle in rabbits in a dose-depended manner.Bay K8644 and nitro-L-arginine methylester(L-NAME)could completely block the inhibition of ginsenoside Rg1 on the contraction of small intestine smooth muscle.Ginsenoside Rg1 inhibited the intracellular calcium-depended contraction induced by rynodine in the Ca2+ free Tyrode's solution.Conclusions Ginsenoside Rg1 inhibits the contraction of small intestine smooth muscle of rabbits in vitro.The mechanism may be related to increase NO concentration in small intestine smooth muscle so that it inhibits extracellular Ca2+ inflowing via cell membrane and intracellular Ca2+ releasing via sarcoplasmic reticulum.
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Aim To define the effect of genistein (GST) on ceruloplasmin (CP) expression in cerebral cortex of focal cerebral ischemia male rats.Methods The effect of GST on CP expression were investigated by means of immunohistochemistry and Western blot in cerebral cortex of focal cerebral ischemia male rats.Results The expression of CP was time coursed during brain ischemia. According to the sham group,CP expression decreased in 6 h-,12 h-and 24 h-ischemia groups,and then increased gradually in 48 h-and 72 h-ischemia rats. GST weakened the ischemia-induced CP change.Pretreatment with an antiestrogen tamoxifen (TAM) could completely abolish the effect of GST.Conclusion The present results indicate that GST may inhibit the time coursed expression changes of CP and then provide neuroprotective effects by inhibiting iron related oxidative stress during brain ischemia via estrogen receptor.
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Aim To observe the effects of theaflavin on intracellular calcium concentration(i) level in rat ventricular myocytes and discuss the possible mechanisms.Methods The effects of theaflavin oni were investigated in rat ventricular myocytes.i was detected by laser confocal microscopy and represented by relative fluorescent intensity(FI-FI0)/FI0,%;FI0:control;FI:administration of drugs).Results ① Theaflavin(10,20,40 ?mol?L-1) had no effect on the i of ventricular myocytes in normal Tyrode′s solution.However,it reduced the i of ventricular myocytes in simulated ischemia solution in a concentration-dependent manner.② Pretreatment with Bay k8644(0.5 ?mol?L-1) mostly abolished the effects of theaflavin(20 ?mol?L-1) in simulated ischemia solution.③ Theaflavin(20 ?mol?L-1) markedly inhibited the low concentration of ryanodine-induced i increase in Ca2+-free Tyrode′s solution.④ When the propagating waves of elevated i(Ca2+ waves) were produced by increasing extracellular Ca2+ concentration from 1 mmol?L-1to 10 mmol?L-1,theaflavin(20 ?mol?L-1) could block the propagating waves of elevated i(Ca2+ waves),reduce the frequency and duration of propagating waves,and reduce i as well.Conclusion Theaflavin may reduce the i in isolated rat ventricular myocytes via inhibiting Ca2+ influx by voltage-dependent Ca2+ channel and alleviating Ca2+ release from sarcoplasmic reticulum(SR).