| Background and objective: Intracerebral hemorrhage(ICH) is characterized by high disability and mortality rate around the world, and there is still no effective treatment up to now. Recent studies have shown that the cerebral tissue had an ability to remove hematoma after ICH, and the hematoma absorption rate was positively correlated with neurologic deficit scores(NDS). Recently, few studies have shown that perihematoma inflammation could influence the hematoma absorption. In addition, the secondary damage caused by the inflammation is an important reason for the aggravated NDS after ICH. Therefore, elucidating the mechanism of how inflammation affects hematoma absorption may provide a new target for promoting hematoma absorption treatment ICH.B type scavenger receptor CD36 has played a key role in mediating cell phagocytosis. Previous studies have shown that microglia promotes phagocytosis of the erythrocyte and its ingredients through CD36.Our previous study has found that the inflammatory cascade activated by hematoma componentsdown-regulated the expression of microglia CD36, which further reduced the hematoma removal and delayed the recovery of neural function in ICH mice. At the same time, our clinical small sample study found that the hematoma absorption slowed in patients with ICH with CD36 mutation, suggesting that CD36 plays an important role in promoting hematoma absorption and affects the neurologic function, but it remains to be confirmed by a larger sample clinical research.Methods and results: 349 patients with ICH admitted to Xinqiao hospital and Xi’nan hospital was generated from July 2012 to June 2014.The National Institutes of Health Stroke Scale score(NIHSS) was measured at admission and on days 7, 14 and 30, and the modified Rankin Scale(m RS) score was evaluated at 3 months after ICH. Serum samples were obtained on 5 and 14 days to detect the levels of interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α). Meanwhile, venous blood was collected to screen 35 cases of CD36 mutation patients using the PCR-SSP technology. 24 basal ganglia region ICH patients were selected from the 35 of CD36 mutation cases and divided into CD36-deficiency group. Meanwhile, 24 of CD36 normal ICH patients who have similar characters with the CD36-deficency group were selected as the CD36-normal group. The hematoma absorption, inflammatory responses and NDS of the two group patients were compared.35 cases with CD36-deficiency were screened out of 349 cases with ICH(10.03%). There was no significant difference in the age, hematoma volume on admission, blood glucose, blood pressure and other baseline data of the two group patients(P > 0.05). Comparing the two groups hematoma absorption rate at 7 days after ICH, we found that the hematoma absorption rate of CD36-deficiency patients was significantly lower than that of the CD36-normal patients(22.4±2.4% vs. 44.8±5.1% CD36-normal; P < 0.05). Comparing with the CD36 normal patients, at the 14, 30 and 90 days after ICH, the NDS of CD36-deficiency patients were higher than the CD36-normal patients(P < 0.05). In addition, the reduction rate of pro-inflammatory factors in CD36-deficiency at 14 days after ICH were higher than that in CD36-normal patients(P < 0.05).Conclusions: This study found that CD36 deficiency was existing in the ICH patients, and further confirmed that CD36 may have an important role in promoting the hematoma absorption after ICH. Thus, this may provide a novel idea of promoting hematoma absorption treatment ICH. |
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