Role of H2S produced by CSE in cerebral ischemia-reperfusion injury in mice and its relationship with RhoA-ROCK2 signaling pathway / 中国药理学通报

Aim To investigate the role of H2S pro¬duced by CSE in cerebral ischemia-reperfusion ( I/R) injury and its relationship with RhoA-ROCK2 signaling pathway.Methods Bilateral common carotid artery ligation was used to prepare a mouse cerebral ischemia- reperfusion injury model.Laser speckle method was used to detect cerebral blood flow, HE staining method was used to observe the pathological changes of brain hippocampus, and the activity of LDH, NSE, RhoA and ROCK,, H,S content and ROCK, protein expres¬sion were detected.Results The H,S synthase CSE substrate L-Cys ( 3(X) mg • kg-1) could significantly promote the recovery of cerebral blood flow in brain 1/ R mice, improve the pathological damage of hippocam¬pus , inhibit the increase of LDH activity in serum and NSE, RhoA and ROCK2 activity in brain tissues, and inhibit the decrease of serum H2S content and the in¬crease of ROCK2 protein expression in brain tissues.But the above effects of L-Cys could be significantly at¬tenuated by the CSE inhibitor PPG (50 mg • kg~ 1 ) ; the H2S donor NaHS (4.8 mg • kg"1 ) also had the same effect as L-Cys did.Conclusions H2S pro¬duced by CSE has a protective effect on mouse brain 1/ R injury, and its effect may be related to inhibiting RhoA-ROCK signaling pathway and increasing cerebral blood flow.

Determination of H2S in rat brain tissues by GC-MS based on bispentafluorobenzyl sulphide / 中国药理学通报

Aim To establish a method for the determination of hydrogen sulfide ( H2S) in rat brain tissues by gas chromatogra- phy-mass spectrometry (GC-MS) on bispentafluorobenzyl sulfide ( C6F5CH2SCH2C6F5 ).Methods Chromatographic conditions: Hie column was HP-5MS(30 m x 250 jxm x 0.25 |xm) and temperature programmed, the injection port temperature was 280 V..Mass spectrometry conditions: The electron bombardment ion source was 20 eV.'Hie ion source, quadrupole and interface temperature was kept at 230.150 and 280 XI, respectively, The MRM mode was used to quantitatively and qualitatively analyze the C6F5CH2SCH2C6F5 ion pair (m/z 394->181, m/z 181->161 ), Results The concentration of sodium hydro- sulfide( NaHS) in brain tissue samples had good linearity in the range of 0.25 ~256 jxmol • L~'.'Hie limit of detection was 0.1 jxmol • L~'.'Hie intra-day and inter-day precision were both less than 15%.There was no obvious matrix effect and the recover)' rate was more than 90%.'Hie H2S concentration in brain tissues could be selectively determined.'Hie basic H2S concentration in rat brain cortex was measured to be ( 11.84 ±0.38) jxmol • L_l.After intravenous injection of NaHS.the H2S concentration in brain tissues increased significantly in a dose-de- pendent manner.Conclusions The GC-MS method based on C6F5CH2SCH2C6F3 established here is reliable and effective to investigate H2S in brain tissues, and H2S could enter brain tissues through the blood-brain barrier.

Role of S-sulfhydration of RhoA kinase in neuroprotection of hydrogen sulfide against hypoxic injury / 中国药理学通报

Aim To investigate the role of S-sulfhydration of RhoA kinase 2 in the neuroprotection of hydrogen sulfide (H2S) against hypoxic injury. Methods Rat hippocampal neurons were primarily cultured and treated with exogenous H2S donor NaHS (50, 100, 200 (xmol • L"1 ) and S-sulfhydration inhibitor DTT (50 (xmol • L"1 during 4 hours of hypoxia and 12 hours of reoxygenation. Cell viability, the lactate dehydrogenase (LDH) activity and neuron-specific enolase (NSE) activity released from injured neuron to culture supernatant, and the proportion of apoptotic cells were measured to assess the neuroprotection of H2S, and the role of S-sulfhydration in the neuroprotection of H2S was preliminarily explored. In addition, the S-sulf- hydrated proteins in neurons were isolated and purified by modified biotin-switch assay. And then, the RhoA kinase 2 (ROCK2) expression and activity, and S-sul- fhydrated ROCK2 were detected to further confirm the role H2S on the S-sulfhydrated ROCK2 by Western blot and assay kits, respectively. Results The decrease of cell viability, and the increase of LDH and NSE released from injured neuron to culture supernatant and cell apoptosis after hypoxia/ reoxygenation ( H/R) were significantly inhibited by 100 and 200 |imol • L"1 NaHS. Compared with the effect of 200 jimol • L"1 NaHS, the neuroprotection of 200 (xmol • L"1 NaHS could be inhibited by co-application with DTT. Furthermore, 100 and 200 (junol • L"1 NaHS could reduce the expression of R0CK2 protein and restrain ROCK2 activity via promoting the S-sulfhydryl modification of ROCK2 protein in hippocampal neurons. Conclusions H2S exerts protective effect on H/R injury of rat hippocampal neurons via down-regulation of ROCK2 expression and inhibition of R0CK2 activity by S-sulfhydration modification.

Effect of CBS-derived H2S from mouse nerve cells on proliferation and migration of brain microvascular endothelial cells and its relationship with VEGFR2 / 中国药理学通报

Aim To study the effect of H2S synthase CBS-derived H2S from mouse nerve cells on the proliferation and migration of the brain vascular endothelial cells and its relationship with VEGFR2. Methods CCK-8 method was used to detect cell proliferation, cell scratch method and Transwell method were used to detect cell migration, methyl blue method was used to detect H2S content, and calcium fluorescence imaging method was used to detect intracellular free Ca2 + concentration. HT22 cells were co-cultured with bEnd. 3 cells by using Transwell system. Results The H2S donor NaHS( 1 xlO"8-1 X 10"3'5 mol • L'1) significantly increased the proliferation and migration of HU- VEC cells and bEnd. 3 cells, while the VEGFR2 blocker SU5416 (10 (xmol • L"1) markedly inhibited the NaHS- increased proliferation and migration; in the co-culture system,the substrate of H2S synthase CBS, L-Cys (100 |xmol • L"1) , significantly promoted the proliferation and migration of bEnd. 3 cells, and increased intracellular Ca2 + fluorescence intensity in bEnd. 3 cells and the H2S content in the co-culture. However, CBS inhibitor AO A A (1 mmol • L"1 ) and SU5416 significantly attenuated the effects of L-Cys on the proliferation and migration and intracellular Ca2 + fluorescence intensity. Conclusions The CBS-derived H2S from neurons can promote the proliferation and migration of mouse cerebral vascular endothelial cells, which may be related to activation of VEGFR2 and subsequently increase of intracellular free Ca2+ concentration.

Quality of realgar and its influencing factors based on toxicity / 中国中药杂志

The results of a toxicity analysis showed differences from those of the existing experimental data. Therefore, HPLC-ICP-MS was used to analyze the soluble arsenic content at different valences in realgar prepared with water grind processing, which were collected from 3 companies. The results showed that the free arsenic of the 3 companies did not exceed the limit of Chinese Pharmacopoeia. However, if the free arsenic was calculated based on the total value of As(Ⅲ) + As(Ⅴ), free arsenic of 1 company exceeded the limit of Chinese Pharmacopoeia. The method of determining free arsenic in Chinese Pharmacopoeia. was ancient Cai's arsenic detection method, which had a certain limitation and failed to effectively avoid the toxicity of remaining arsenics except for trivalent arsenic. Then, we examined the effects of water and temperature on the content and form of soluble arsenic in realgar. The results showed that the content of soluble arsenic increased with the rise of water content, and the form of soluble arsenic did not change, there were only As (Ⅲ) and As (Ⅴ); With the simple temperature factor, there was an increasing trend in the content of soluble arsenic in the samples, the maximum increment was As (Ⅲ) 2.489 mg•g⁻¹ and As (Ⅴ) 0.546 mg•g⁻¹; When water and temperature played an synergistic effect, the increase of soluble arsenic in the samples significantly changed, the maximum increment was As (Ⅲ) 23.690 mg•g⁻¹, As (Ⅴ) 0.468 mg•g⁻¹, respectively. Through comprehensive analysis, we believed that the quality of realgar was susceptible to water content and temperature. Both of the single effect of water content and the synergistic effect of water and temperature can significantly change the content of soluble arsenic in realgar, and the water content was a high-risk factor. In the current Chinese Pharmacopoeia 2015 version, the free arsenic detection method had limitations, hence new techniques shall be introduced; At the same time, realgar does not have a water content inspection item in the current pharmacopoeia, which shall be added. However, due to the limit of water content, more in-depth studies are required.

Protective effects of Sapindus saponins in spontaneously hypertensive rats / 中国结合医学杂志

<p><b>OBJECTIVES</b>To investigate the protective effects of Sapindus saponins in spontaneously hypertensive rats, and the possible cellular and molecular mechanisms.</p><p><b>METHODS</b>Thirty-two 16-week-old spontaneously hypertensive rats were randomly divided into four groups (8 in each group): model group (placebo), positive control group (27 mg/kg of Captopril Tablets), Sapindus saponins groups (27 mg/kg and 108 mg/kg, respectively). Another 8 healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for 8 weeks. Blood pressure of rats was determined by non-invasive blood pressure meter (BP-6). Furthermore, the contents of angiotensin II (Ang II) in plasma and myocardial tissue were determined by enzyme-linked immunosorbent assay (ELISA), the gene expression of receptor angiotensin type 1 (AT1R) in aorta was determined by quantitative realtime polymerase chain reaction (qRT-PCR). The protein expression of transforming growth factor-β1 (TGF-β1) and AT1R in heart was determined by immunohistochemical staining. The protein expression of p-phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK) was determined by Western blotting. The contents of interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF) in serum were determined by radioimmunoassay. And the histopathological and morphological changes of aorta and heart tissue samples were assessed semi-quantitatively by hematoxylin-eosin (HE) or Masson staining.</p><p><b>RESULTS</b>Thirty minutes after single or continuous treatment, systolic blood pressure (SBP) was reduced significantly in Sapindus saponins groups. And the contents of AngII, IL-1, IL-6 and TNF-α in serum, the expression of AT1R mRNA, p-p38MAPK and TGF-β1 were significantly suppressed dose-dependently (P<0.05 or P<0.01). With the Sapindus saponins treatment, compared with those of the model group, the cardiac and aortic pathological changes were ameliorated significantly.</p><p><b>CONCLUSIONS</b>Our findings suggest that Sapindus saponins might have protective effects in spontaneously hypertensive rats, the cellular and molecular mechanisms of which might be relevant to the regulation of inflammatory responses mediated by p-p38MAPK signal pathway based on activated Ang II and AT1R.</p>

Protective effect against myocardial ischemia reperfusion injuries induced by hyperoside preconditioning and its relationship with PI3K/Akt signaling pathway in rats / 中国中药杂志

To investigate the protective effect of preconditioning with hyperoside ( Hyp) against myocardial ischemia-reperfusion injury (MIRI) in rats and the role of PI3K/Akt signaling pathway. MIRI was established by ligation of left anterior descending coronary artery for 30 min followed by reperfusion for 120 min in rats. Male SD rats were randomly divided into five groups: sham group,model group (MIRI),Hyp preconditioning group(Hyp), Hyp preconditioning + LY294002 (a PI3K/Akt signaling pathway inhibitor) group (Hyp + LY), and LY294002 group (LY). At the end of reperfusion, hemodynamic parameters were recorded as left ventricular systolic pressure (LVSP) , left ventricular end-diastolic pressure ( LVEDP) and maximal rate of increase and decrease of left ventricular pressure (± dP/dt(max)). Myocardial infaret size, the oxidative stress markers, myocardial enzymes indicators and inflammatory factors were also analyzed. The expressions of Akt, p-Akt, Bax and Bcl-2 proteins was detected by using Western blot method. The results showed that Hyp preconditioning remarkably improved cardiac constriction and relaxation function, reduced myocardial infarct size and enhanced the activities of oxidative stress markers about correlated to MIRI, such as superoxide dismutase (SOD), catalase (CAT) and glutathione-peroxidase (GSH-Px) and decreased the contents of malondialdehyde (MDA) as compared with MIRI group. Simultaneouly, the levels of myocardial enzymes, i. e. creatine kinase ( CK) and creatine kinase MB isoenzyme (CK-MB), and inflammatory factors, for instance tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were decreased. Hyp pretreatment apparently restrained myocardial apoptosis as evidenced by decreasing the level of Bax expression, increasing the levels of phosphorylation of Akt and Bcl-2 expression. These effects were inhibited by LY294002, a blocker of PI3K/Akt signaling pathway. These findings indicated that the cardioprotection of Hyp preconditioning against MIRI may be related to activating PI3K/Akt signaling pathway, upregulating the expression of BCL-2 protein and down-regulating the expression of Bax protein.

Effects and mechanisms of hyperoside on vascular endothelium function in middle cerebral arteries of rats ex vivo / 中国中药杂志

To investigate the effects and potential mechanisms of hyperoside (Hyp) on the vascular endothelium function in middle cerebral artery (MCA) ex vivo in rats. Isolated arterial segments from MCAs of rats were used for surveying vasomotoricity in a pressurized chamber. Transmembrane potential was recorded by using glass microelectrodes to evaluate hyperpolarization. Hyp (1 x 10(-6)-1 x 10(-4) mol . L-1) was utilized to observe the effect on 1 x 10(-7) mol . L-1 U46619-preconstricted MCA in rats. The results showed that 1 x 10(-6)-1 x 10(-4) mol . L-1 Hyp significantly induced concentration-dependent vasodilatation and hyperpolarization, leading to the maximal diastolic ratio of (73. 2 ± 6. 1)% and maximal changes in membrane potentials of (-13. 2 ± 2. 2) mV. Hyp still elicited vasorelaxation and hyperpolarization by removal of endothelium in MCA of rat, which was notably attenuated as compared with vascular endothelium-intact group (P <0. 01). In the MCAs preconstricted by U46619 (1 x 10(-7) mol . L-1), Hyp (1 x 10(-6)-1 x 10(-4) mol . L-1) produced concentration-dependent vasorelaxation and hyperpolarizition that were partially attenuated by 3 x 10(-5) mol . L-1 L-NAME(a NOS inhibitor) plus 1 x 10(-5) mol . L-1 PGI2 ,(a synthetase inhibitor). The residual effects were further decreased by 1 x 10(-3) mol . L-1 TEA (an inhibitor of Ca2+-activated potassium channel) or 1 x 10(-5) mol . L-1 PPG (a blocker of endogenous H2S synthese-CSE). Similarly, 1 x 10(-5)-1 x 10(-3) mol . L-1 NaHS (a donor of exogenous H2S) or 1 x 10(-5)-1 x 10(-3) mol . L-1 L-Cys (the substrate of endogenous H2S synthesis) obviously evoked dose-dependent vasodilatation and hyperpolarization of MCA in rats. These findings indicated that Hyp may induce endothelium-dependent and endothelium-independent responses. And the endothelium-dependent vasodilatation may be related to the increases of endogenous H2S that has been promoted Hyp in the endotheliocyte of MCAs, and activated Kca and opening of Kca channels, resulting in the hyperpolarization of vascular smooth muscle cell membrane and subsequent reduction of Ca2+ influx and vasodilation.

Effects of sapindus saponins on inflammatory response mediated by Ang II/p38MAPK pathway and cardiac hypertrophy in spontaneously hypertensive rats / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the effects of sapindus saponins on myocardial inflammation mediated by Ang II/ p38MAPK signal pathway and cardiac hypertrophy in spontaneously hypertensive rats. And also to explore the correlation of cardiac hypertrophy and inflammation.</p><p><b>METHOD</b>Thirty-two 16-week-old spontaneously hypertensive rats (SHR) were randomly divided into four groups, one with placebo as model group, one with captopril tablets (27 mg x kg(-1)) as positive control, one with low-dose sapindus saponins (27 mg x kg(-1)), one with high-dose (108 mg x kg(-1)). And another eight healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for eight weeks, and the indicators detected were as follows: (1) left ventricular mass index (LVMI); (2) the content of Ang II and hs-CRP in plasma were determined by ELISA; (3) the protein expression of AT1R and VEGF were determined by immunohistochemical method; (4) the protein expression of p-p38MAPK in myocardial cells was determined by Western blot.</p><p><b>RESULT</b>Sapindus saponins reduced LVMI, and blocked the expression level of Ang II, AT1R, p-p38MAPK, VEGF and hs-CRP in myocardial tissue. Vs the SHR model group, there were significant differences (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Our findings suggested that sapindus saponins could inhibited cardiac hypertrophy, the possible mechanisms may be related to the inhibition on inflammatory response mediated by Ang II/p38MAPK pathway.</p>

Research of sapindus saponins on endothelial function in spontaneously hypertensive rats / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the regulation on endothelial function of sapindus saponins in spontaneously hypertensive rats by studying the reactivity on different vasoconstrictor and dilator, and the content of the active substances.</p><p><b>METHOD</b>Forty 16-week-old spontaneously hypertensive rats were randomly divided into five groups, one with placebo as model group, one with captopril tablets (27 mg x kg(-1)) as positive control, one with low-dose sapindus saponins (27 mg x kg(-1)), one with medium-dose (54 mg x kg(-1)), one with high-dose (108 mg x kg(-1)). And another eight healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for eight weeks, and the indicators to be detected were as follows: (1) the response of thoracic aorta on different vasoconstrictors Ang II (1 x 10(-9) -1 x 10(-5) mol x L(-1)), PE (1 x 10(-8) 1 x 10(-4) mol x L(-1)), KCl (20 -120 mmol x L(-1)); (2) the endothelium-dependent or non-endothelium-dependent vasodilation response of thoracic aorta on Ach (1 x 10-(10)-1 x 10(-5) mol x L(-1)) or SNP (1 x 10(-8)-1 x 10(-3) mol x (L(-1); (3) the content of NO, 6-KPG1alpha, ET-1 and TXB2 in serum was determined by Elisa.</p><p><b>RESULT</b>In SHR model group, the response of thoracic aorta on Ang II, PE and KCl was increased, the endothelium-dependent vasodilation on Ach was reduced, but the effects on SNP was not obvious, the content of ET-1 and TXB2 was increased, and the content of NO and 6-KPG1alpha was reduced, Vs the normal control group, there were significant differences (P < 0.05 or P < 0.01); in the treatment groups, the response of thoracic aorta on Ang II, PE and KCl was reduced, the endothelium-dependent vasodilation of thoracic aorta on Ach was improved, the content of ET-1 and TXB2 was reduced, and the content of NO and 6-KPG1alpha was increased, Vs the SHR model group, there were significant differences (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Our findings suggested that sapindus saponins protected the endothelial function in SHR, the mechanisms were relevant to the protection of endothelial function.</p>

Effects of remifentanil on intracellular Ca(2+) and its transients induced by electrical stimulation and caffeine in rat ventricular myocytes / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Preconditioning with remifentanil confers cardioprotection. Since Ca(2+) overload is a precipitating factor of injury, we determined the effects of remefentanil on intracellular Ca(2+) ([Ca(2+)](i)) and its transients induced by electrical stimulation and caffeine, which reflects Ca(2+) handling by Ca(2+) handling proteins, in rat ventricular myocytes.</p><p><b>METHODS</b>Freshly isolated adult male Sprague-Dawley rat myocytes were loaded with Fura-2/AM and [Ca](i) was determined by spectrofluorometry. Remifentanil at 0.1 - 1000 microg/L was administered. Ten minutes after administration, either 0.2 Hz electrical stimulation was applied or 10 mmol/L caffeine was added. The [Ca(2+)](i), and the amplitude, time resting and 50% decay (t(50)) of both transients induced by electrical stimulation (E [Ca(2+)](i)) and caffeine (C [Ca(2+)](i)) were determined.</p><p><b>RESULTS</b>Remifentanil (0.1 - 1000.0 microg/L) decreased the [Ca(2+)](i) in a dose-dependent manner. It also decreased the amplitude of both transients dose-dependently. Furthermore, it increased the time to peak and t(50) of both transients dose-dependently.</p><p><b>CONCLUSION</b>Remifentanil reduced the [Ca(2+)](i) and suppressed the transients induced by electrical stimulation and caffeine in rat ventricular myocytes.</p>

Protective effect of injection of Danhong against acute myocardial ischemia in dogs / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the protective effects of injection of Danhong against acute myocardial ischemia in dogs.</p><p><b>METHOD</b>The myocardial ischemia model were established by ligation of coronary artery in dogs. The degree of myocardial ischemia and the myocardial infarction size were observed before and after giving injection of Danhong. The serum creatine phosphokinase (CK) and lactate dehydrogenase (LDH) activities were also determined.</p><p><b>RESULT</b>Injection of Danhong (1, 2, 4 g x kg(-1)) could significantly decreased the damage degree of myocardial ischemia, redused myocardial infarction size and also reduced the serum LDH and CK activities.</p><p><b>CONCLUSION</b>Injection of Danhong had protective action on myocardial ischemia.</p>

Protective effect of urantide against myocardial ischemia injury / 药学学报

This study is to investigate the protective effect of urantide against myocardial ischemia injury in mice and its mechanism. The ischemic model was made by using subcutaneous injection of isoproterenol (Iso) in mice, the change of ST segment of electrocardiogram (ECG) was observed, and the activitise of lactate dehydrogenase (LDH) and nitric oxide synthetase (NOS), the contents of malonaldehyde (MDA) and nitric oxide (NO) in serum were measured. The histopathological changes of myocardium were observed by using HE staining. The anoxia/reoxygenation (A/R) model of myocardial cells on neonatal Sprague-Dawley rats was established. Methyl thiazolyl tetrazolium (MTT) assay and confocal microscopy were respectively used to measure the viability and intracellular Ca2+ concentration in myocardial cells exposed to A/R. LDH activity and cTnI content in the cell culture medium were assayed for the evaluation of myocardial cells injury. The results revealed that urantide in the range of 3 - 30 microg kg(-1) iv markedly inhibited Iso-induced raise of the ST segment of ECG; 10 and 30 microg kg(-1) significantly reduced the increases of MDA content and LDH activity in mice serum, remarkably raised the activity of NOS and the content of NO. Urantide (10 and 30 microg kg(-1)) also significantly ameliorated myocardial ischemic injury. On the A/R model of myocardial cells, urantide (1 x 10(-6) - 1 x 10(-9) mol L(-1)) could evidently inhibit the increases of cTnI content, reduce the rise of intracellular Ca2+ concentration. Urantide (1 x 10(-6) - 1 x 10(-7)) mol L(-1) increased the viability of myocardial cells injured by A/R and cut down LDH activity in the cell culture medium. Therefore urantide has significant protective effect against myocardial ischemia or A/R injury via the inhibition of Ca2+ overload and the augmentation of NO synthesis.

Role of p38 mitogen-activated protein kinases in cardioprotection of morphine preconditioning / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>p38 mitogen-activated protein kinases (MAPK) in ischemic preconditioning (IPC) may be essential to cardioprotection. We assessed whether protective effect of morphine-induced preconditioning (MPC) on myocardial ischemia and reperfusion injury in rat hearts involved p38 MAPK activation.</p><p><b>METHODS</b>Male Spargue-Dawley rats (weighing 300-350 g) were randomly assigned to 1 of the following 8 groups: control (CON, saline vehicle, n=9), SB 203580 (SB, a p38 MAPK inhibitor, n=6), MPC (n=6), IPC (n=9), SB+MPC, SB+IPC, MPC+SB, and IPC+SB (n=6). Infarct sizes (IS), a percentage of the area at risk (AAR), were determined by triphenyltetrazolium (TTC) staining. Tissue samples were processed from the entire AAR of left ventricle for the determination of p38 MAPK protein expression (5 hearts/group). The bands representing the proteins were visualized using an enhanced chemiluminescence detection system.</p><p><b>RESULTS</b>The IS/AAR was significantly reduced by IPC (12.9+/-1.6)% or MPC (25.3+/-2.9)% compared to the control (52.7+/-5.5)%. SB 203580 administered prior to preconditioning abolished the effect of IPC (SB+IPC: (43.8+/-2.6)%, P>0.05 vs CON, P<0.01 vs IPC), but not MPC (SB+MPC: (30.7+/-0.9)%, P<0.01 vs CON, P>0.05 vs MPC). Treatment with SB 203580 prior to sustained ischemia diminished the protective effect of both MPC (MPC+SB: (42.4+/-2.9)%, P>0.05 vs CON) and IPC (IPC+SB: (52.0+/-2.5)%, P>0.05 vs CON) on IS/AAR. In the IPC group, phospho-p38 MAPK protein increased significantly within 5 minutes into ischemia and remained elevated at 30 minutes into reperfusion, while phospho-p38 MAPK protein in the MPC group only increased significantly at 30 minutes into reperfusion.</p><p><b>CONCLUSION</b>The activation of p38 MAPK just acts as a mediator of MPC, whereas it acts as both a trigger and a mediator in IPC.</p>

Effects of total flavone of Abelmoschl Manihot L. Medic on the function of platelets and its mechanism / 中国结合医学杂志

<p><b>OBJECTIVE</b>To study the effects of total flavone of Abelmoschl Manihot L. Medic (TFA) on the function of platelets and to explore its mechanism.</p><p><b>METHODS</b>Rat models of artery-veins bypassing thrombus formation were used. The platelets of rabbits were collected. Platelet aggregation was induced by collagen and intracellular calcium ion concentration ([Ca(2+)]i) was assayed by Fura-2 method.</p><p><b>RESULTS</b>TFA (25, 50, 100 mg/kg) significantly and dose-dependently reduced the weight of thrombus. TFA (0.025, 0.05, 0.1 mg/ml) possessed dose-dependant inhibitory effects on rabbits' platelet aggregation induced by collagen. TFA significantly reduced the resting and CaCl(2)-induced increase of free intracellular calcium concentration ([Ca(2+)]i) in rabbit platelet in vitro.</p><p><b>CONCLUSION</b>TFA has an antiplatelet effect via the inhibition on the influx of Ca(2+).</p>

Anti-aging action of the total lactones of ginkgo on aging mice / 药学学报

<p><b>AIM</b>To investigate the effects of total lactones of ginkgo on aging by using D-galactose induced aging mice and natural aging mice.</p><p><b>METHODS</b>By using D-galactose induced aging mice, to detect the LF content in heart and liver, the Hyp content in liver, the MAO, GSH-Px activities and the NO content in cerebrum. The apoptosis of cerebral cell was determined by terminal deoxy-nucleotidyl transforase-mediated dUTP-digoxigenin nick end-labeling (Tunel) in natural aging mice.</p><p><b>RESULTS</b>TLG was shown to increase the GSH-Px activities, reduce the NO content and decrease the MAO activity in cerebrum. Meanwhile, TLG was found to reduce the LF content in liver and heart and raise the Hyp content in liver. TLG was shown to inhibit apoptosis of cerebral cell and decrease the number of apoptotic cells in the brain.</p><p><b>CONCLUSION</b>TLG possesses effect on antiaging via attenuating lipid peroxidation and NO and apoptosis of cerebral cells.</p>