Salvianolic acid a inhibits platelet activation and aggregation in patients with type 2 diabetes mellitus

Zhou, Aiming; Xiang, Yijia; Liu, En-Qian; Cai, Changhong; Wu, Yuning; Yang, Lebing; Zeng, Chunlai

doi:10.1186/s12872-019-01316-z

Cited by 15 publications

(11 citation statements)

References 29 publications

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“…Salvianolic acid A (Sal‐A) is the key bioactive water‐soluble constituent of Salvia miltiorrhiza 15,16 . Studies have also verified that Sal‐A owned massive pharmacological function containing antioxidation, 17 antiplatelet aggregation 18 and against ischaemia/reperfusion injury 19 . Sal‐A increases vasoconstriction by regulating the transgelin‐actin complex 20 .…”

Section: Introductionmentioning

confidence: 99%

Salvianolic acid A blocks vasculogenic mimicry formation in human non‐small cell lung cancer via PI3K/Akt/mTOR signalling

Jin

Chen

Huang

et al. 2021

Clin Exp Pharma Physio

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Vasculogenic mimicry (VM) is associated with aggressive cancer cells. Salvianolic acid A (Sal‐A), an antioxidant and anti‐inflammatory agent, has bioactive properties from Salvia miltiorrhiza Bunge. Current investigation aspired to explore the activity of Sal‐A in the VM formation of non‐small cell lung cancer (NSCLC) and the mechanism underling this function. The CCK8, the scratch and boyden chemotaxis assay were presented to describe NSCLC cells viability, migration and invasion capabilities, respectively. The protein expression was verified by western blotting. In this report, Sal‐A caused a reduction in viability, metastasis and capillaries structure formation of NSCLC cells. Additionally, Sal‐A markedly prevented the key VM related proteins, containing EphA2, VE‐cadherin and MMP2. Besides, Sal‐A significantly diminished p‐PI3K, p‐Akt and p‐mTOR level in NSCLC cells. More importantly, SC79 pretreatment reversed Sal‐A inhibits NSCLC cells viability, metastasis and VM formation. These data exhibit that Sal‐A could block VM network formation in NSCLC cells through modulating the PI3K/Akt/mTOR signalling pathway.

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Section: Introductionmentioning

confidence: 99%

Salvianolic acid A blocks vasculogenic mimicry formation in human non‐small cell lung cancer via PI3K/Akt/mTOR signalling

Jin

Chen

Huang

et al. 2021

Clin Exp Pharma Physio

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“…Each freeze-dried sample was resuspended in 4 mL of PPP. The concentration of fresh platelets was adjusted to 10×10 9 /L with PBS. The samples were incubated with PAC-1 and CD62P for 15 min at room temperature.…”

Section: Determination Of the Expression Levels Of Cd62p And Pac-1 By Three-colour Flow Cytometrymentioning

confidence: 99%

“…Several studies have confirmed that these two indicators can be used in the monitoring and early prevention of platelet activation in hypercoagulable diseases. 9 As a new type of hypoglycaemic drug, glucagon-like peptide-1 (GLP-1) receptor agonists have received increasingly more attention in recent years. In addition to lowering blood sugar, these drugs also showed good effects in reducing the cardiovascular risk of T2DM.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Exenatide on Coagulation and Platelet Aggregation in Patients with Type 2 Diabetes

Zhang¹,

Chen²,

Jia³

et al. 2021

DDDT

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To explore the effect of the glucagon-like peptide-1 receptor agonist exenatide on coagulation function and platelet aggregation in patients with type 2 diabetes mellitus (T2DM). Methods: Thirty patients with newly diagnosed T2DM were enrolled as the case group, and 30 healthy people with matching age and sex were selected as the control group. Patients in the case group received exenatide treatment for 8 weeks. The general clinical data and biochemical indicators of all subjects were collected; and their peripheral blood platelet count, coagulation index, nitric oxide (NO), platelet membrane glycoprotein (CD62p), platelet activation complex-1 (PAC-1) and platelet aggregation induced by collagen, epinephrine (EPI), arachidonic acid (AA), and adenosine diphosphate (ADP) were detected. Results: The fibrinogen, CD62p, PAC-1, and platelet aggregation rates of the case group (pretreatment) are higher than those in the control group (EPI 77.90±6.31 vs 60.15±5.37, ADP 52.89±9.36 vs 47.90±6.16, and AA 76.09±3.14 vs.55.18±3.55); and the NO level is lower in the case group than in the control group (p<0.05, respectively). After 8 weeks of exenatide treatment in the case group, the CD62p, PAC-1, and platelet aggregation rates were lower than before the treatment (EPI: 61.96±8.94 vs 77.90±6.31 and AA: 50.98±6.73 vs 76.09±3.14); and the NO level was higher than before the treatment (p<0.05, respectively). Pearson correlation analysis showed that the changes in platelet aggregation rates (Δ EPI and ΔAA) of the patients in the case group after 8 weeks of exenatide treatment were positively correlated with the changes in body mass index, waist circumference, weight, blood lipids, fasting plasma glucose, haemoglobin A1c, fibrinogen, CD62p, and PAC-1 and negatively correlated with the changes in high-density lipoprotein and NO (p<0.05). Multiple linear regression analysis showed that the changes in NO, CD62p and PAC-1 were independent risk factors affecting the changes in platelet aggregation rates. Conclusion:The GLP-1R agonist exenatide can inhibit the activation state of platelets in patients with T2DM and inhibit thrombosis, which is beneficial to reduce the risk of cardiovascular events.

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“…PAC-1 is the GPIIb/IIIa complex brinogen receptor. Several studies have con rmed that these two indicators can be used in the monitoring and early prevention of platelet activation in hypercoagulable diseases [9].…”

Section: Introductionmentioning

confidence: 99%

Effects of Exenatide on Blood Coagulation and Platelet Aggregation in Patients with Type 2 Diabetes

Zhang

Chen

Jia

et al. 2021

Preprint

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Background: To explore the effect of glucagon-like peptide-1 receptor (GLP-1R) agonist exenatide on blood coagulation function and platelet aggregation function in patients with type 2 diabetes mellitus (T2DM).Method: Thirty patients with newly diagnosed T2DM were enrolled as the case group, and 30 healthy people with matching age and sex were selected as the control group. Patients in the case group received exenatide treatment for 8 weeks. Collect the general clinical data and biochemical indicators of the patients in the case group before and after 8 weeks of exenatide treatment and the control subjects, and detect their peripheral blood platelet count (×1012 g/L), plasma prothrombin time (PT, s), prothrombin time activity (PTA, %), activated partial thromboplastin time (APTT, s), international normalized ratio (INR), fibrinogen (FIB, g/L), plasma thrombin time (TT, s) , Fibrin degradation products (FDP, μg/mL), D-dimer (DD, μg/mL), nitric oxide (NO, μmol/L), CD62p (%), platelet activation complex-1 (PAC-1, %) and platelet aggregation induced by collagen, epinephrine, arachidonic acid (AA, %), and adenosine diphosphate (ADP, %).Results: There was no significant difference in platelet count, PLT, PT, PTA, APTT, TT, INR, FDP, DD between the case group and the control group; the FIB, CD62p, PAC-1, platelet aggregation rates of the case group (EPI 87.23±6.84 , ADP 87.51±9.21, AA 90.17±3.19) is higher than normal control group (EPI 82.15±5.37, ADP 82.38±6.42, AA 83.41±6.17, P＜0.05), NO level is lower than normal control group (68.1±14.7 vs. 79.4±11.2, P<0.05); After 8 weeks of exenatide treatment in the case group, CD62p, PAC-1, and platelet aggregation rates were lower than before (EPI: 81.62±9.02 vs. 87.23±6.84, AA: 84.62±7.12 vs. 90.17±3.19, P＜0.05), the level of NO was higher than before (89.6±15.8 vs. 68.1±14.7); Pearson correlation analysis showed that the changes in platelet aggregation rates (Δ EPI, ΔAA) of patients in the case group after 8 weeks of exenatide treatment were positively correlated with the changes in body mass index (BMI, kg/m2), waist circumference (cm), weight (kg), total cholesterol (TCH, mmol/L), triglycerides (TG, mmol/L), low-density lipoprotein (LDL-C, mmol/L), fasting plasma glucose (FPG, mmol/L), Hemoglobin A1c (HbA1c, %), CD62p, PAC-1 (P<0.05), and negatively correlated with the change of high density lipoprotein (HDL-C, mmol/L) and NO (P<0.05). Multiple linear regression analysis showed that the changes of NO, CD62p and PAC-1 were independent risk factors affecting the changes of platelet aggregation rates.Conclusions: The GLP-1R agonist exenatide can inhibit the activation state of platelets in patients with T2DM, reduce the platelet aggregation rate, and inhibit thrombosis, which is beneficial to reduce the risk of cardiovascular events.

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Salvianolic acid a inhibits platelet activation and aggregation in patients with type 2 diabetes mellitus

Cited by 15 publications

References 29 publications

Salvianolic acid A blocks vasculogenic mimicry formation in human non‐small cell lung cancer via PI3K/Akt/mTOR signalling

Salvianolic acid A blocks vasculogenic mimicry formation in human non‐small cell lung cancer via PI3K/Akt/mTOR signalling

Effects of Exenatide on Coagulation and Platelet Aggregation in Patients with Type 2 Diabetes

Effects of Exenatide on Blood Coagulation and Platelet Aggregation in Patients with Type 2 Diabetes

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