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.

Correlation of peripheral blood T cell changes with nerve damage, inflammatory response and stress response in patients with acute cerebral infarction

Objective: To investigate the correlation of peripheral blood T cell changes with nerve damage, inflammatory response and stress response in patients with acute cerebral infarction. Methods: 108 patients with acute cerebral infarction who received emergency treatment in Xuefu Hospital of Shaanxi Normal University between September 2015 and August 2017 were selected as the cerebral infarction group, and 100 healthy elderly volunteers who underwent physical examination during the same period were selected as the normal control group. The differences in the expressions of CD4+CD25+ regulatory T lymphocytes in peripheral blood as well as the levels of nerve damage indicators, inflammatory factors and oxidative stress indicators in serum were compared between the two groups. Pearson test was used to evaluate the intrinsic relationship between peripheral blood CD4+CD25+ regulatory T lymphocyte expression and infarction condition in patients with acute cerebral infarction. Results:Peripheral blood CD4+CD25+ regulatory T lymphocyte expression of the cerebral infarction group was higher than that of the normal control group;serum nerve damage indicators UCH-L1, GFAP, and Ang-1 levels were higher than those of the normal control group while IGF-1 and BDNF levels were lower than those of the normal control group;serum inflammatory factors IL-1β, VCAM-1, IL-13, and IL-18 levels were higher than those of the normal control group;serum oxidative stress indicators CAT and T-SOD levels were lower than those of the normal control group whereas MDA level was higher than that of the normal control group. Correlation analysis confirmed that peripheral blood CD4+CD25+ regulatory T lymphocyte expression in patients with acute cerebral infarction was directly correlated with the levels of nerve damage indicators, inflammatory factor, and oxidative stress indicators. Conclusion:The abnormal increase of peripheral blood CD4+CD25+ regulatory T lymphocyte expression in patients with acute cerebral infarction is related to the aggravation of nerve damage and systemic inflammatory stress response.