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Objective: To analyze the clinical application of manual therapy (MT) to tumor-related adverse reactions via summarizing the research at home and abroad, in order to provide more theoretical evidence for the clinical promotion of MT. Methods: We searched 7 Chinese and English databases, including China National Knowledge Infrastructure (CNKI), Wanfang Academic Journal Full-text Database (Wanfang), Chongqing VIP Database (CQVIP), PubMed, Excerpta Medica Database (EMBASE), Ovid and EBSCO. The publication date was between the establishment date of the database and December 31, 2020. We screened the literature according to the inclusion and exclusion criteria, and then sorted and analyzed the selected information. Results: A total of 46 papers were analyzed. Most studies focused on the adverse reactions in breast cancer patients. MT interventions demonstrated the best efficacy for fatigue, followed by pain, depression and anxiety. In different MT interventions, Tuina (Chinese therapeutic massage) was mainly adopted for fatigue, pain, anxiety, depression, and limb dysfunctions. Acupoint pressing was mainly adopted for gastrointestinal and psychological problems such as abdominal bloating, insomnia, depression and anxiety. The application of reflexotherapy was similar to that of Tuina. Conclusion: MT can alleviate various adverse reactions by effectively relieving patients' somatic symptoms and improving their psychological states and overall functions. It can be popularized as a significant non-drug therapy. Currently, however, the clinical application of MT is neither extensive nor has sufficient basic research. Consequently, we should attach importance to this application.
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[ ABSTRACT] AIM:To investigate the cardiac AMP-activated protein kinase ( AMPK) activity and the effects of AMPK activator on cardiac structure and function in the mice with different β-adrenoceptor (β-AR) stimulation patterns . METHODS:Male BALB/c mice were subcutaneously injected with AMPK activator ( AICAR, 250 mg· kg -1 · d-1 ) or saline, and infused with β-AR agonist isoproterenol (ISO, 5 mg· kg-1· d-1) for 14 d.The cardiac functions were evalu-ated by echocardiography or hemodynamic method , and the hearts were harvested after infusion cessation immediately or 3 d later.Phosphorylated AMPK ( p-AMPK) was measured by Western blot .RESULTS:Sustained ISO infusion increased p-AMPK level.AICAR did not further increase p-AMPK but attenuated ISO-induced increase in heart weight .Sustained ISO infusion increased cardiac systolic function as indicated by left ventricular fractional shortening ( FS) and maximum rate of pressure rise (+dp/dtmax).The cardiac systolic function was not further increased by AICAR .The cardiac diastolic func-tion as indicated by left ventricular end-diastolic pressure (LVEDP) was not different in each group .In contrast, cardiac p-AMPK level was similar between the control mice and the mice with sustained ISO infusion and ceased infusion for 3 d. In this model, AICAR improved the cardiac systolic and diastolic functions , which were impaired by ISO.Moreover, the increased pattern of p-AMPK level was similar with that of heart rate upon ISO stimulation .CONCLUSION: Sustained ISO infusion increases p-AMPK.After ISO infusion cessation for 3 d, p-AMPK is decreased to the basal level .β-AR-in-duced inotropic effects should be avoided to investigate the cardioprotective role of AMPK activation in the β-AR stimulation models.
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OBJECTIVE To investigate the blocking activities of a series of potential α1-adrenoceptor (α1-AR) antagonists (Compounds B1 -B9) on α1-AR.METHODS ① A series of potential α1-adrenoceptor (α1-AR) antagonists,indolylpiperidine derivative (IPD) and Compounds B1 -B9,with indolylpiperidine moiety and different substitutes were synthesized through the coupling of indolylpiperidine and piperazine derivatives.② Inotropic responses experiment was used to examine blocking effects of IPD and Compounds B1 - B9 in isolated rat atria by phenylephrine (PE) stimulation.③ Blocking effect of IPD and Compounds B1 - B9 on phosphorylation level of extracellular signal-regulated kinase (ERK) in PE treated HEK293 cells was tested by Western blotting.RESULTS ① Potential α1-adrenoceptor (α1-AR) antagonists with indolylpiperidine moiety and different substitutes were synthesized successfully.② PE caused a dose-dependent inotropic response which was inhibited by pre-incubation of phentolamine (Phen),a non-selective α1-AR antagonist,IPD and Compounds B1,B3,B4,B7,B8 and B9,respectively; IPD and Compounds B4 and B8 caused an obvious rightward shift of inotropic response-curve,the pA2 values for IPD and Compounds B4 and B8 were 6.72 ± 0.21,6.86 ± 0.29 and 6.67 ± 0.19,respectively.③ Phosphorylation level of ERK1/2 was inhibited by pre-incubation with Compounds B1,B2,B3,B5,B6,B7,B8 and B9 or IPD in PE treated α1A-AR stably expressed HEK293 cells; PE-stimulated phosphorylation level of ERK1/2 was inhibited by pre-incubation with Compounds B2,B4,B7 or B8 in α1B-AR stably expressed HEK293 cells.CONCLUSION Compound B4 has a selective blocking activity on α1B-AR,and Compounds B1,B3,B5,B6 and B9 or IPD have a selective blocking activity on the phosphorylation level of ERK1/2.
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To determine which subtype of alpha1-adrenergic receptors plays a role in the regulation of blood pressure, with alpha1A-adrenergic receptor-mediated vasoconstriction in perfused hindlimb as a control, we compared the inhibitory effects of various alpha1-adrenergic receptor selective antagonists on the vasopressure responses to phenylephrine between the mean arterial pressure and hindlimb perfusion pressure in anesthetized rats. In Normotensive Wistar rats, the results showed that the inhibitory effects (dose ratios of ED50, Dr) of alpha1-adrenoceptor selective antagonist (prazosin, Dr 13.5+/-3.6 vs.15.1+/-4.3, n = 11), alpha1A-adrenoceptor selective antagonist (5-methyl-urapidil, Dr 2.4+/-0.9 vs. 3.7+/-2.3, n = 12; RS-17053, Dr 3.2+/-1.6 vs. 4.4+/-3.3, n =12) and alpha1D-adrenoceptor selective antagonist (BMY7378, Dr 1.9+/-0.9 vs. 2.2+/-0.8, n=8) on phenylephrine- induced increases of perfusion pressure in the autoperfused femoral beds were the same as that in the mean arterial blood pressure in normotensive Wistar rats. The inhibitory effects of antagonists (RS-17053, Dr 3.4+/-0.6 vs. 4.3+/-0.9, n = 5; BMY7378, Dr 1.7+/-0.5 vs. 1.7+/-0.5, n = 8) in spontaneous hypertensive rats were similar with the Wistar rats. These results suggest that the mean arterial pressure induced by phenylephrine was mainly mediated by alpha1A-adrenergic receptor in both the anesthetized Wistar rats and spontaneous hypertensive rats.
Subject(s)
Adrenergic alpha-Agonists/pharmacology , Blood Pressure/drug effects , Blood Pressure/physiology , Phenylephrine/pharmacology , Receptors, Adrenergic, alpha-1/drug effects , Receptors, Adrenergic, alpha-1/physiology , Adrenergic alpha-Antagonists/pharmacology , Animals , Hypertension/drug therapy , Hypertension/physiopathology , Indoles/pharmacology , Male , Piperazines/pharmacology , Rats , Rats, Inbred SHR , Rats, Wistar , Receptors, Adrenergic, alpha-1/classificationABSTRACT
Objective: To better understand the antagonistic effect of Xiao Long Tong Bi (XLTB), a Chinese herb medicine, on α1-adrenoceptor (α1-AR). Methods: (1) Radio ligand binding assay . Specific 125I-BE2254(2-β(4-hdroxyphenyl)-ethyl amino-methyl-tetralone) binding was measured by incubating membrane of canine cerebral cortex with a single concentration of 125I-BE2254 in the presence of 15 concentrations of XLTB. Half-effectual concentration of inhibition (IC50) and Hill coefficients (nH) were determined by Hill plots. (2) Contractile responses of rat prostate strip in vitro were determined. pKB values for XLTB in competitively inhibiting NE-stimulated contraction of tissues were measured by the method of Ainlakshana. Results: XLTB competitively inhibited binding of 125I-BE2254 to α1-AR in a concentration -dependent manner. IC50 values for XLTB in canine cerebral cortex were (34.0±6.0) g*L-1, the Hill efficiency value (0.7±0.1) was significantly decreased from unity. Contractile studies showed that XLTB competitively antagonized the NE concentration-response curve with pKB values of (37.0±11.0) g*L-1 or (30.0±8.0) g*L-1 when XLTB concentration was 70 g*L-1 or 170 g*L-1, respectively. The pKB values for XLTB in antagonizing NE-induced contraction of tissues were showed to fit in well with the IC50 values on rat prostate. Conclusion: These results suggest that XLTB appears to be a competitive antagonist for α1-AR.