RESUMO
ObjectiveTo explore the clinical effect of Tiaoxin formula in the treatment of patients with coronary heart disease and anxiety/depression and its impact on serum levels of 5-hydroxytryptamine （5-HT）， β- thromboglobulin （β-TG） and myeloperoxidase （MPO）. MethodA total of 66 patients with coronary heart disease and anxiety/depression were randomly divided into the Tiaoxin formula group and Deanxit group， 33 cases in each group. Both groups were given fundamental western treatment for coronary heart disease. Additionally， the Deanxit group was treated with flupentixol and melitracen tablets and the Tiaoxin formula group was treated with Tiaoxin Formula. The treatment lasted 8 weeks. Before and after treatment， the changes of clinical efficacy， Patient Health Questionnaire （PHQ-9）， Generalized Anxiety Disorder （GAD-7） scale， Seattle Angina Questionnaire （SAQ）， heart rate variability， and serum 5-HT， β-TG and MPO levels， and incidence of adverse reactions in the two groups were observed. ResultThere was no significant difference in the baseline indexes of patients in the two groups， and thus the two groups were comparable. After treatment for 8 weeks， the total effective rate for traditional Chinese medicine （TCM） syndromes in the Tiaoxin Formula group was 87.88% （29/33） higher than 63.64% （21/33） in the Deanxit group （Z=-2.653， P<0.05）. Compared with those before treatment， the PHQ-9 and GAD-7 scores of the two groups were decreased at week 4 and 8 of treatment （P<0.05）， and there was no statistical difference between two groups. And the SAQ dimension scores of the two groups were increased at week 4 and 8 of treatment （P<0.05）. Compared with the Deanxit group， the Tiaoxin Formula group had elevation in two dimension scores： Physical limitation and angina stability （P<0.05）. Compared with the conditions before treatment， the serum 5-HT level in the two groups were increased， while the β-TG and MPO levels were lowered （P<0.05）， and there was no distinct difference between two groups. In addition， the standard deviation of normal-to-normal intervals （SDNN） and standard deviation of average normal-to-normal intervals （SDANN） of the heart rate variability in the Tiaoxin formula group were elevated after treatment （P<0.05）， which were more significant than those of the Deanxit group （P<0.05）. During the treatment period， the incidence of adverse drug reactions in the Tiaoxin formula group was lower than that in the Deanxit group （P<0.05）， and no adverse events were observed in the two groups. ConclusionTiaoxin formula was effective for the treatment of patients with coronary heart disease accompanied by anxiety and depression， which improved the clinical symptoms， increased serum 5-HT levels， and decreased serum β-TG and MPO levels， and had few adverse reactions and high safety for patients， showing a high clinical value.
RESUMO
Objective@#To explore the influence of high-voltage electrical burns on the number of platelet aggregation, β-thromboglobulin (β-TG) and platelet factor 4 (PF-4) and the interventional effects of ulinastatin in rats with high-voltage electrical burns.@*Methods@#A total of 240 Sprague-Dawley rats were divided into sham injury (SI) group, simple electrical burn (SEB) group, normal saline (NS) group, and ulinastatin (UTI) group according to the random number table, with 60 rats in each group. The electrical current was applied to the outside proximal part of left forelimb of rats and exited from the outside proximal part of right hind limb of rats. Rats in groups SEB, NS, and UTI were inflicted with high-voltage electrical burn wounds of 1 cm×1 cm at current entrances and exits, with the voltage regulator and experimental transformer. Rats in group SI were sham injured through connecting the same equipments without electricity. At 2 min post injury, rats in group NS were intraperitoneally injected with 2 mL/kg NS, and rats in group UTI were intraperitoneally injected with 2×104 U/kg UTI of 10 g/L. At 15 min before injury and 5 min, 1 h, 2 h, 4 h, 8 h post injury, 10 rats in each group were selected to collect 5-7 mL blood of heart respectively. Blood of 0.05 mL were collected to make fresh blood smear for observing the number of platelet aggregation, and serum were separated from the remaining blood to determine content of β-TG and PF-4 with enzyme-linked immunosorbent assay. Data were processed with analysis of factorial design of variance, student-Newman-Keuls test, Kruskal-Wallis H test, Wilcoxon rank sum test, and Bonferroni correction.@*Results@#(1) At 15 min before injury, the numbers of platelet aggregation of rats were close among groups SI, SEB, NS and UTI (5.9±1.2, 5.8±1.2, 5.9±1.3, 5.9±1.1, respectively, with P values above 0.05). At 5 min, 1 h, 2 h, 4 h, 8 h post injury, the numbers of platelet aggregation of rats in group SEB were 57.2±16.3, 59.1±16.9, 60.8±20.6, 83.6±24.9, and 83.4±30.3, respectively, obviously more than those in group SI (6.0±1.3, 6.0±1.4, 5.9±1.4, 5.7±1.1, and 5.8±1.3, respectively, with P values below 0.001); the numbers of platelet aggregation of rats in group UTI were 29.6±7.4, 31.9±10.1, 35.0±14.2, 43.0±13.6, and 35.2±11.1, respectively, obviously more than those in group NS (58.3±16.1, 63.9±18.0, 60.8±17.7, 74.2±23.0, and 82.3±21.9, respectively, with P values below 0.001). There was no significantly statistical difference in the number of platelet aggregation of rats in group SI between each two time points within the same group (with P values above 0.05), but the number of platelet aggregation of rats in the other 3 groups at each time point post injury was significantly more than that of the same group at 15 min before injury (with P values below 0.001). (2) At 2, 4, and 8 h post injury, β-TG content of serum of rats in group SEB was significantly higher than that in group SI (with Z values from -3.780 to -3.477, P values below 0.05). At 5 min and 4 h post injury, β-TG content of serum of rats in group UTI was significantly lower than that in group NS (with Z values respectively -3.477 and -3.780, P values below 0.05). There was no significantly statistical difference in β-TG content of serum of rats in group SI at all time points of the same group (χ2=0.130, P >0.05). At 2, 4, and 8 h post injury, β-TG content of serum of rats in group SEB was significantly higher than that of the same group at 15 min before injury (with Z values from -3.780 to -3.553, P values below 0.05). At 5 min, 1 h, and 4 h post injury, β-TG content of serum of rats in group NS was significantly higher than that of the same group at 15 min before injury (with Z values from -3.780 to -3.477, P values below 0.05). At 1 and 4 h post injury, β-TG content of serum of rats in group UTI was significantly higher than that of the same group at 15 min before injury (with Z values respectively -3.250 and -3.780, P values below 0.05). (3) At 2 and 8 h post injury, PF-4 content of serum of rats in group SEB was significantly higher than that in group SI (with P values below 0.05). At 2 h post injury, PF-4 content of serum of rats in group UTI was significantly higher than that in group NS (P<0.05), and at 4 and 8 h post injury, PF-4 content of serum of rats in group UTI was significantly lower than that in group NS (with P values below 0.05). At all time points, PF-4 content of serum of rats in group SI was close (with P values above 0.05). At 2 and 8 h post injury, PF-4 content of serum of rats in group SEB was significantly higher than that of the same group at 15 min before injury (with P values below 0.05). At 1, 4, and 8 h post injury, PF-4 content of serum of rats in group NS was significantly higher than that of the same group at 15 min before injury (with P values below 0.05). There were significantly statistical differences in PF-4 content of serum of rats between all time points except for 5 min post injury and 15 min before injury (with P values below 0.05).@*Conclusions@#Increasing number of platelet aggregation and abnormal secretion of β-TG and PF-4 of rats with high-voltage electrical burns can lead to microcirculation disturbance. UTI can alleviate microcirculation disturbance caused by high-voltage electrical burns by reducing the number of platelet aggregation and inhibiting secretion of β-TG and PF-4.
RESUMO
Objective To unravel the relationship between Toll-like receptor 4 (TLR4) expression in platelets and the activation of platelet in thrombocytopenia (TCP) in case of sepsis. Method A total of 64 patients with sepsis were prospectively studied with control. Platelet count (PC), mean platelet volume (MPV),platelet distribution width (PDW),platelet TLR4 expression, platelet PAC-1 expression, sCD40L and TNF-α concentrations were compared between healthy control group (15 cases) and sepsis group on admission and 3 d,Sd,and 9 days after admission. The changes of MPV and PDW in TCP and non-TCP subgroups of sepsis before and after treatment were recorded. Prognostic index was analyzed. Results The PC was lower in sepsis group (P=0.006), and MPV and PDW were higher in sepsis group than those in healthy control group (P = 0.046, P =0.001). Platelet TLR4 and PAC-1 expressions, and sCD40L and TNF-α levels also increased more significantly in sepsis group (P ＜ 0.001). PAC-1 expression and TNF- level were higher in TCP group than those in non-TCP group before and after treatment (P = 0.023, P = 0.011). The sCD40L concentration and platelet TLR4 expression were significantly higher in treated TCP groups than in non-TCP group (P = 0.047, P = 0.001). Compared with non-TCP,the rate of bleeding was higher (P = 0.024) and the length of ICU stay was longer (P = 0.013).The APACHE Ⅱ score and the 28-day mortality were higher in TCP group (P ＜ 0.01, P = 0.048). Conclusions The elevation of platelet TLR4 expression in sepsis along with platelet activation is closely related to the incidence of thrombocytopenia. The occurrence of TCP is a poor prognosis sign of sepsis.
RESUMO
Objective To affirm the expression of Toll like receptor 4 (TLR4) on the surface membrane of platelet and to explore the immunomodulatory factors[(interlukine-8(IL-8),β-thromboglobulin(β-TG), soluble CD40 ligand(sCD40L)] released by platelets after platelets stimulated by TLR4 ligand.Methods TLR4 expressed on the platelet was detected by flow cytometry. Monoclonal anti-human FcγRⅡantibody(Ⅳ.3)-treated human platelets were cultured with LPS in the presence or absence of blocking monoclonal antibody to human TLR4. The release of IL-8, β-TG, sCD40L were measured by specific enzymelinked immunosorbent assay. Results Human platelets could express functional TLR4. The detection rate of TLR4 on platelets were decreased after LPS involvement(P<0.01). It was noted that sCD40L and β-TG were present in large concentration in the release of platelets stimulated by TLR4 ligand but the release of IL-8 was independent of platelet activation after TLR4 engagement. The concentration of sCD40L and β-TG had no statistical difference between 1-5 μg/ml LPS. The effects of LPS on the modulation of secretory factors were attenuated by preincubation of platelets with an anti-TLR4 monoclonal antibody. Conclusion The TLR4 on platelet could recognize and link LPS, induce the release of sCD40L, β-TG by platelet, but could not influence IL-8.