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Aim To investigate the expression of stro-mal interaction molecule 1 (STIM1) in rat pulmonary arterial hypertension ( PAH ) tissues and effects of STIM1 on arterial muscle cells proliferation. Methods PAH was induced by a single intraperitoneal injec-tion of MCT at a dose of 60 mg·kg - 1 . The mRNA or protein expressions of STIM1 in monocrotaline-induced pulmonary hypertensive rats were measured by real-time PCR or Western blot, respectively. The arterial smooth muscle cells A7R5 were transiently transfected with STIM1 plasmids to prepare STIM1 overexpressed cells. Cell proliferations were detected by using CCK-8 kits. The expressions of Akt/ mTOR pathway molecules of A7R5 were measured by Western blot. Results The right ventricular systolic blood pressure ( RVSP) and right ventricular mass index ( RVMI ) were markedly elevated in MCT-treated rats (P < 0. 01) in comparison to control rats. The mRNA and protein ex-pression levels of STIM1 in monocrotaline-induced pul-monary hypertensive rats were 2. 19 and 1. 66 folds of control rats, respectively. STIM1 were transiently over-expressed in cultured A7R5. Cells transfected with STIM1 grew more quickly than non-transfected control. Overexpression of STIM1 significantly increased the phosphorylation of Akt, mTOR, p70-S6K, and 4E-BP1, but did not change their protein expression lev-els. Conclusion STIM1 are over-expressed in rat PAH tissues. Overexpression of STIM1 can promote ar-terial smooth muscle cells proliferation by regulating Akt/ mTOR pathway.
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The transient receptor potential( TRP) subfamilies be-long to the non-selective cation channels located at cell mem-branes. Calcium across the plasma membrane into the cell via most TRP channels may result in localized Ca2+ signals that con-tribute to cell proliferation, migration and metastasis. In recent years, many studies have focused on the role of TRP in cancer. This review intends to gather the latest progress concerning TRP channels on proliferation and migration of cancer.
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Aim To evaluate the effects of notoginsen-oside R1 on store-operated calcium entry ( SOCE ) in pulmonary arterial smooth muscle cells ( PASMCs ) of chronic hypoxia ( CH)-and monocrotaline ( MCT)-in-duced pulmonary hypertension ( PH) rats. Methods Mn2+ quenching of Fura-2 and measurement of intra-cellular free calcium concentration ( [ Ca2+] i ) using fluo-3 were examined in PASMCs of CH-exposed and MCT-treated rats. Results ①CH-exposed and MCT-treated rats exhibited profound PH when examined 3 weeks after hypoxia exposure or MCT injection, respec-tively. ②In the presence of 3 μmol·L-1 nifedipine, 10 μmol · L-1 notoginsenoside R1 significantly re-duced cyclopiazonic acid ( CPA )-induced the percent reduction in Fura-2 fluorescence measured 500 sec af-ter application of Mn2+, the maximal rate of Mn2+quenching, the amplitude of the Ca2+ influx transient and the resting [ Ca2+] i in PASMCs of CH-exposed and MCT-treated rats. Conclusion Notoginsenoside R1 inhibits SOCE and reduces resting [ Ca2+] i in PASMCs of CH-and MCT-induced PH rats.
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Aim Tostudytheeffectsofferulicacid (FA) on doxorubicin (DOX) induced cellular injury inH9c2ratmyocardialcells.Methods H9c2cells were treated with 1μmol·L-1 DOX treated for 24 h to establish a myocardial injury model. 10, 20, 40μmol ·L-1 FA was added 2 h before DOX treatment. Cell viability was measured by cell counter kit ( CCK-8 ) . Morphological changes were observed by phase contrast microscope. LDH, CK, MDA, SOD levels were detec-ted by biochemical kits. Intracellular level of reactive oxygen species ( ROS) was examined by DCF-DA stai-ning with flow cytometry. Cellular apoptosis was detec-ted by AO-EB staining and DNA agarose gel electro-phoresis. The expression of caspase-3, Bax, Bcl-2 was evaluatedbyWesternblot.Results Exposureof H9c2 cells to DOX led to decrease in cell viability, in-crease in stress and apoptosis. FA pre-treatment im-proved cell viability in a dose-dependent manner, at-tenuated leakage of LDH and CK, and reversed mor-phological changes induced by DOX. FA suppressed DOX-induced oxidative stress as evidenced by reducing ROS and MDA generation and increasing SOD enzyme activity. FA depressed myocardial apoptosis by down-regulating pro-apoptotic protein caspase-3 and Bax, whereas up-regulating apoptosis inhibitory protein Bcl-2.Conclusions FAhasaprotectiveeffectonDOX-induced injury in H9c2 cells. This protection may re-sult from inhibition of myocardial oxidative stress and apoptosis.
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Aim To evaluate the time-course curve of expression of TRPC1 and vascular tone of pulmonary arteries(PAs)mediated by SOCE in chronic hypoxia pulmonary hyperte-nsion rats.Methods Both tension of PA rings and expression of TRPC1 were tested in CH exposure (1 0.0 % ±0.5 %partialpressure ofoxygen ) induced pulmonary hypertensive (PH)rats,and the time-course curve(detected respectively in CH 1 ,3,5, 7,1 4,21 d)was traced.Results ①CH could up-regulate the mean right ventricular pressure(mRVSP) ,which was increased significantly on 1 d,and reached the maximum on 7d;right ventricular weight index (RV-MI)began increase on 3d,and kept rising;②semi-quantitative reverse transcription polyme-rase chain reaction (RT-PCR)was performed to detect the expression of TRPC1 in PAs.The expression of TRPC1 increased significantly on 1 d,and reached the maxi-mum on 3d;③CH could up-regulate the vascular tone of PAs mediated by SOCE,which was increased signif-icantly on 3d,and reached the maximum on 7d.Con-clusions TRPC1 /SOCE increases significantly in the early days of CH,and the time-course curve of the two has correlation,which reflects the important role of the upregulation of TRPC1 /SOCE in the process of chronic hypoxia pulmonary hypertension.
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The second edition physiology published by People's Health Publishing House has been re-drawn and added many illustrations. The illustrations of the new version have improved significantly in the clarity,aesthetics,science,information-rich,etc.It will help to improve the quality of teaching.Some experiences can be got by drawing: First, it is necessary to fully understand the physiological knowledge.Second,one of reference materials should be selected as a template to make creative working.Third,some basic principles should be followed,such as reasonable layout,appropriate grayscale,rich content,simple composition,etc.
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The combination of teachers'leading role and the students'main role is a basic principle of teaching. This paper discusses how to play the leading role of teachers from pre-teaching preparation and classroom teaching to coaching students and answering the questions after school..
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AIM To study the characteristics of Ca 2+ channel mediated store operated Ca 2+ influx on rat vascular smooth muscle. METHOD Fura 2 fluorescence technique was used to investigate the [Ca 2+ ] i change. RESULTS ① S nitrosocaptopril (CapNO,20～120 ?mol?L -1 ) produced a concentration dependent inhibitory effect on cyclopiazonic acid(CPA) induced [Ca 2+ ] i change. The maximal inhibitory effect(37%?17%) of CapNO was reached at a concentration of 80 ?mol?L -1 . The same concentration of Captopril had no effects. ② Inhibition rate of 80 ?mol?L -1 CapNO (The concentration of maximal effect, CME) on CPA induced [Ca 2+ ] i change was 30%?10%, subsequent addition of 1 ?mol?L -1 Nif (CME)did not further produced the decrease effect (54%?18%). subsequent addition of 20 ?mol?L -1 SK&F96365 (CME) further produced the decrease effect. The inhibitory effects of 20 ?mol?L -1 SK&F96365 were significantly different in the cases of CapNO and Nif pretreatment(24%?10%) and non treatment (54%?11%). ③ The inhibitory effects of 2 ?mol?L -1 tyrphostinAG490(AG490,CME) were significantly different in the cases of CapNO (CME) pretreatment (24%?9%)and non treatment (42%?10%). 80 ?mol?L -1 CapNO effect on CPA induced [Ca 2+ ] i changes in AG490 pretreatment condition(18%?7%) was different from that in non treatment case(37%?10%). CONCLUSION S nitrosocaptopril obviously inhibits the opening of SOCC and VDCC, which mediates store operated Ca 2+ influx. The inhibitory effects of CapNO is associated with both sensitive to and non sensitive to tyrosine kinase (Janus2).