Effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction

Objective: To study the effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction. Methods:The patients with massive cerebral infarction who received treatment in our hospital between January 2016 and December 2017 were selected and randomly divided into the group A receiving Butylphthalide treatment, the group B receiving Urinary Kallidinogenase treatment and the group C receiving Butylphthalide combined with Urinary Kallidinogenase treatment on the basis of conventional treatment. 14 d after treatment, serum levels of nerve markers, coagulation indexes, growth factors and oxidative stress indexes were determined. Results:After treatment, visinin-like protein-1 (VILIP-1), neuron-specific enolase (NSE), S100B protein (S100B), thromboxane A2 (TXA2), lysophosphatidic acid (LPA), D-dimer (D-D), 8-isoprostanes F2α (8-iso-PGF2α) and malondialdehyde (MDA) levels of 3 groups significantly decreased whereas nitric oxide (NO), nitric oxide synthase (NOS), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) levels significantly increased, and VILIP-1, NSE, S100B, TXA2, LPA, D-D, 8-iso-PGF2α and MDA levels of the group C after treatment were significantly lower than those of the group A and group B whereas NO, NOS, VEGF, BDNF, IGF-I, SOD and T-AOC levels were significantly higher than those of the group A and group B. Conclusion: Butylphthalide combined with Urinary Kallidinogenase is better than monotherapy in improving the pathological course of nerve damage in patients with massive cerebral infarction.

Meta-analysis of the clinical efficacy and safety of Urinary Kallidinogenase in the treatment of acute cerebral infarction

Objective:To evaluate the clinical efficacy and safety of Urinary Kallidinogenase for Injection in the treatment of acute cerebral infarction.Methods:PubMed,The Cochrane Library,Embase,CNKI,VIP,Wan Fang and bibliographic database of Chinese medicine were searched by computer to collect randomized controlled trials of Urinary Kallidinogenase's treatment of acute cerebral infarction.The time limit was set up until September 2019.At the same time,the references and grey literature in the literature were manually screened.Two independent researchers were screened,evaluated and extracted according to inclusion and exclusion criteria.Meta-analysis was carried out by RevMan 5.3 software.Results:A total of 17 randomized controlled trials involving 2,066 patients,including 1,033 in the experimental group,and 1,033 in the control group.meta-analysis results showed that compared with the conventional treatment,Urinary Kallidinogenase had better effect in the treatment of acute cerebral infarction[OR=3.26,95%CI(2.56,4.16),P<0.00001];the national institule of Health Stroke Scale of the Urinary Kallidinogenase group was significantly better than that of the control group.Urinary Kallidinogenase group activity of daily living scale was better than the control group[OR=21.33,95%CI(6.64,36.01),P=0.004];a total of 7 articles reported adverse reactions,including 19 cases in the trial group and 21 cases in the control group,the main adverse reactions were blood pressure drop,other symptoms were chest tightness,facial redness,dizziness fever,nausea and vomiting,arrhythmia,and no other serious adverse reactions.It can recover itself.Conclusion:the available evidence shows that Urinary Kallidinogenase can effectively improve the symptoms of neurological deficits and improve the ability of daily living in patients with acute cerebral infarction,and is safe.However,the quality of the study is limited.

Effects of Urinary Kallidinogenase combined with mNGF on neurotrophic status, apoptosis and oxidative stress in patients with ischemic stroke

Objective:To study the effects of Urinary Kallidinogenase combined with mouse nerve growth factor (mNGF) on neurotrophic status, apoptosis and oxidative stress in patients with ischemic stroke.Methods: Patients with acute ischemic stroke who were treated in Jiangmen Central Hospital between March 2015 and October 2017 were selected and divided into two groups according to random number table method, the control group received conventional therapy, and the observation group received Urinary Kallidinogenase combined with mNGF therapy on the basis of routine therapy. The contents of neurotrophic cytokines, soluble apoptosis molecules and oxidative stress markers in serum were measured before treatment and 14d after treatment.Results:Serum BDNF, NTF, VEGF, HGF and IGF-1 levels of observation group after treatment were higher than those before treatment whereas serum BDNF, NTF, VEGF, HGF and IGF-1 levels of control group after treatment were not significantly different from those before treatment;serum sFas, sFasL, sTRAIL, 8-OHdG, Hcy and MDA levels of both groups after treatment were lower than those before treatment whereas Livin, Bcl-2, SOD and GSH-Px levels were higher than those before treatment;serum sFas, sFasL, sTRAIL, 8-OHdG, Hcy and MDA levels of observation group after treatment were lower than those of control group whereas BDNF, NTF, VEGF, HGF, IGF-1, Livin, Bcl-2, SOD and GSH-Px levels were higher than those of control group.Conclusion: Urinary Kallidinogenase combined with mNGF can improve the neurotrophic state and inhibit the apoptosis and oxidative stress response in patients with ischemic stroke.

Mechanism of edaravone combined with urinary kallidinogenase for acute cerebral infarction patients

Objective:To observe the effects of edaravone combined with urinary kallidinogenase on serum ox-LDL, PCT, hs-CRP, TNF-α and T cell subsets in patients with acute cerebral infarction, so as to explore the mechanisms of combination therapy on patients with acute cerebral infarction. Methods:86 cases of patients with acute cerebral infarction in our hospital from March 2014 to May 2016 were randomly divided into two groups:control group and observation group, 43 cases in each group. All patients were given general treatment according to their own specific conditions, including hypoglycemic, pressure adjustment, prevention and treatment of complications, symptomatic support therapy, etc. The control group were given 30 mg Edaravone Injection on this basis with once per day for 14 d;The observation group was treated with 0. 15 PNA urinary kallidinogenase intravenous drip with once per day for 14 d on the basis of the control group. The levels of serum x-LDL, PCT, hs-CRP, TNF-αand CD3+, CD4+, CD8+, CD4+/CD8+were detected and compared between the two groups. Results:(1) Before treatment, there was no significant difference between the two groups on the levels of serum ox-LDL, PCT, hs-CRP, and TNF-α;after treatment, the serum levels of ox-LDL, PCT, hs-CRP and TNF-αin the two groups were significantly lower than that before treatment, and the difference was significant (P<0.05);(2) Before treatment, there was no significant difference between the two groups on the levels of serum CD3+, CD4+, CD8+, CD4+/CD8+;after treatment, the serum levels of CD3+, CD4+and CD4+/CD8+were significantly increased in the two groups, and the level of CD8+was significantly decreased compared with the same group before treatment, and the difference was significant (P<0.05);and the levels of serum CD3+, CD4+, CD8+and CD4+/CD8+in the observation group were significantly better than those in the control group, and the difference was significant (P<0.05). Conclusions:The treatment of combined application of urinary kallidinogenase and edaravone in patients with acute cerebral infarction, can significantly improve the serum levels of ox-LDL, PCT, hs-CRP, TNF-αand T cell subsets, further illustrates the synergistic effect of the combination, also shows that the two drugs for acute cerebral infarction can inhibit thrombosis to expand, reduce inflammation, relieve cerebral tissue damage, and improve neurological function.