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BACKGROUND: In addition to FUNDC1, Bnip3 and Nix mitochondrial autophagy pathways in mammals that are closely related to the hypoxic environment, Pinkl/Parkin is the main mitochondrial autophagy pathway after brain injury. PINK1 acts upstream of Parkin, and the Pinkl/Parkin pathway is used to mediate loss of mitochondrial surface functional proteins or structural polyubiquitination, and considered as a marker for autophagosome selection, which has an important influence on autophagy-dependent degradation of depolarized mitochondria. OBJECTIVE: To analyze the role of Pinkl/Parkin-mediated mitochondrial autophagy in rats with brain injury after hypertensive intracerebral hemorrhage. METHODS: The study was approved by the Laboratory Animal Ethical Committee of North Sichuan Medical College. Forty-five male Wistar rats of SPF grade were randomly divided into normal, model and autophagy inhibitor groups. The rats in the model and autophagy inhibitor groups were used to prepare hypertensive cerebral hemorrhage model. Before modeling 2 µL of PBS solution containing trimethyl adenine (100 nmol/L) was intraperitoneally injected in the inhibitor group, and the model and the normal groups were intraperitoneally injected with 2 µL of PBS. The water content, mitochondrial autophagy, mitochondrial membrane potential, cerebral infarction, mitochondrial LC3, Parkin protein and PINK1 protein expression in brain tissue were detected. RESULTS AND CONCLUSION: (1) Compared with the normal group, the autophagy staining and mitochondrial staining expression in the model group was increased, and the number of co-localized positive cells was increased (both P < 0.05). Compared with the model group, the autophagy staining and mitochondrial staining expression in the autophagy inhibitor group was decreased, and the number of co-localized positive cells was decreased (both P < 0.05). (2) Compared with the normal group, the infarction proportion of the brain in the model group was increased (P < 0.05). Compared with the model group, the infarction proportion of the brain in the autophagy inhibitor group was increased (P < 0.05). (3) Compared with the normal group, the mitochondrial staining intensity in the model group was decreased, and the autophagy staining intensity was increased (both P < 0.05). Compared with the model group, the mitochondrial staining intensity in the autophagy inhibitor group was decreased, and the autophagy staining intensity was increased (both P < 0.05). (4) Compared with the normal group, the expression levels of PINK1, LC3 and Parkin in the model group were increased (P < 0.05). Compared with the model group, the expression levels of PINK1, LC3 and Parkin in the autophagy inhibitor group were decreased (P < 0.05). In summary, mitochondrial autophagy can alleviate the degree of brain injury after hypertensive intracerebral hemorrhage. The Pinkl/Parkin pathway plays an important role in the mitochondrial autophagy.
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Objective To investigate the influence of hematoma heterogeneity for the enlargement of primary supratentorial intracerebral hemorrhage and established predictive scoring model of hematoma enlargement. Methods From June 2015 to December 2017, a total of 208 patients with primary cerebral hemorrhage treated first at the First Affiliated Hospital of Jishou University were analyzed retrospectively. 3D software was used to conduct hematoma imaging and calculate hematoma volume and surface area. The patients were divided into enlarged hematoma group (n =44) and non-enlarged hematoma group (n = 164) according to whether the hematomas were enlarged or not. The standard deviation of CT value (CTSD) of hematoma and irregular ratio (IR) of hematoma morphology were used to reflect the heterogeneity of hematoma. Univariate analysis and Multivariate Logistic regression analysis were used to analyze the Influencing factors of hematoma enlargement with SPSS 22. 0 software,and the predictive value of predictive scoring model to hematoma enlargement was evaluated with receiver operating characteristic (ROC) curve. Results The incidence of hematoma enlargement in primary cerebral hemorrhage was 21. 2% (44/208). Compared with the non-enlarged hematoma group,the increased volume of hematoma in the enlarged hematoma group increased significantly (15 ± 11 ml vs. 4 ± 6 ml ,t =45. 568,P 2. 0 and CTSD was 10. 85, the heterogeneity of hematomas increased. Multivariate analysis showed that CCS 10 score at admission (OR, 4. 141,95% CI 1. 526 - 11. 237,/'=0. 005) ,CTSDs5 10. 85 (OR, 3. 593,95% CI 1.354 - 9.540, P =0.010), and IR5s2.0 (OR, 93. 487,95%CI 27. 656 -316.012,P<0.01) were the independent risk factors for hematoma enlargement, and based on this,a predictive scoring model of CIG (CTSD,IR,and GCS) was established ROC curve analysis showed that the sensitivity and specificity of CIG score model predicting the hematoma enlargement were 86. 9% and 95. 1% , respectively when the predictive score was 9. 5 score. Conclusion The heterogeneity of hematoma was first quantified by the density heterogeneity and morphological irregularity of hematoma through individualized imaging processing, and a scoring model of hematoma enlargement was established based on this,which provided a new idea for clinical identification of hematoma enlargement.
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Objective To investigate the correlation between serum matrix metalloproteinase-9 (MMP-9) and intracranial pressure after hematoma removal in patients with primary intracerebral hemorrhage (PICH). Methods From January 2015 to June 2017,72 consecutive patients with PICH treated with removal of hematoma + intracranial pressure probe implantation at the Department of Neurosurgery, the Second Affiliated Hospital of Xinjiang Medical University were enrolled retrospectively. They were divided into 3 groups:group A (n=25,intracranial pressure ≤10 mmHg);group B (n=24,intracranial pressure 11-20 mmHg),and group C (n=23,intracranial pressure >20 mmHg) according to the maximum value of monitoring intracranial pressure. The serum MMP-9 levels of all patients were detected using ELISA at 1, 3,5,7 and 14 d after procedure,the volume of cerebral edema was monitored by head CT,and intracranial pressure was continuously observed for 7 d after procedure using the intracranial pressure monitor. Results At 1,3,5,7,and 14 d after removal of the hematomas,the MMP-9 levels in group A were 82 ± 11,117 ± 12,156 ± 14,132 ± 14,and 108 ± 18 mg/L,respectively,and the volumes of brain edema were 15 ± 6,19 ± 7,22 ± 8,19 ± 7,and 17 ± 6 cm3 ,respectively. The MMP-9 levels in group B were 93 ± 14,138 ±13,188 ± 17,153 ± 17,and 134 ± 12 mg/L,respectively,and the volumes of brain edema were 19 ± 7,23 ± 8,30 ± 10,26 ± 8,and 20 ± 7 cm3 ,respectively;the MMP-9 levels in group C were 104 ± 16,199 ± 14,390 ± 22,296 ± 15,and 213 ± 15 mg/L,respectively,and the volume of brain edema were 22 ± 8,30 ± 10,42 ± 12,32 ±19,and 24 ±8 cm3,respectively. There was significant difference between groups (P<0. 05),and there was a moderate positive correlation between the changes of MMP-9 level and the volume of intracranial cerebral edema (r =0. 62,P <0. 01). Conclusion After the removal of the hematomas of primary cerebral hemorrhage, the MMP-9 level in blood serum of the patients was positively correlated with the volume of brain edema,the higher the level of MMP-9,the higher the intracranial pressure.