ABSTRACT
Objective:To explore the efficacy of breaking blood expelling stasis method accelerates hematoma resolution after intracerebral hemorrhage (ICH) and its potential mechanism.Methods:63 ICH patients confirmed by computer tomography (CT) scan from August 2019 to February 2020 were selected as the research objects and randomly divided into control group ( n=29, routine treatment plus placebo) and observation group ( n=34, routine treatment plus breaking blood expelling stasis granules). The changes of neurological function and hematoma volume were observed before and after treatment. At the same time, the ICH rat model was constructed to observe the changes of neurobehavior and hematoma volume after the intervention of breaking blood expelling stasis granules. The expressions of peroxidase proliferator-activated-receptor γ(PPARγ), CD11b and CD36 in the surrounding tissues of hematoma were detected by Western blot on the third day after the intervention. Results:After two weeks of treatment, the National Institutes of Health Stroke Scale (NIHSS) score and hematoma volume of the two groups decreased (all P<0.05), and the NIHSS score and hematoma volume of the observation group were significantly lower than those of the control group (all P<0.05). In addition, the changes of NIHSS score and hematoma volume in the observation group before and after treatment were significantly greater than those in the control group ( P<0.01). In animal experiments, the hematoma volume in the breaking blood expelling stasis group on the 14th day after ICH was significantly smaller than that in the ICH group [(9.8±4.9)mm 3 vs (17.6±6.4)mm 3,P<0.05], and the reduction of hematoma in the breaking blood expelling stasis group on the 7th and 14th day was significantly larger than that in the ICH group [(4.6±2.9)mm 3 vs (-2.1±1.6)mm 3, (14.3±3.8)mm 3 vs (4.2±2.8)mm 3, all P<0.01]. The percentage of right turn on 3rd, 7th and 14th day and the modified Neurological Severity Score (mNSS) on 7th and 14th day in the breaking blood expelling stasis group were lower than those in the ICH group (all P<0.05). Western blot analysis showed that the expressions of CD11b, CD36 and PPARγ in the breaking blood expelling stasis group on the third day after ICH were significantly higher than those in the ICH group (CD11b: 0.78±0.12 vs 0.49±0.11, P<0.05; CD36: 1.16±0.16 vs 0.80±0.11, P<0.05; PPARγ: 0.78±0.11 vs 0.37±0.10, P<0.01). Conclusions:Breaking blood expelling stasis can effectively accelerate intracerebral hematoma clearance and improve neurological outcome after ICH, and the mechanism maybe probably mediated by activating PPARγ and enhanced CD36, CD11b upregulation on microglia/macrophages, which resulting in facilitating erythrocyte endogenous phagocytosis.
ABSTRACT
Primary biliary cholangitis (PBC) is an autoimmune liver disease characterized by nonsuppurative inflammation of the small- and medium-sized bile ducts in the liver. The pathogenesis of PBC remains unclear, and immunoregulation may play a critical role. As the important components of the immune system, cytokines may be involved in the pathogenesis of PBC. This article reviews related research advances in recent years, including the roles of pro-inflammatory cytokines (interleukin-12, interleukin-17, interleukin-9, interleukin-8, tumor necrosis factor-α, and interleukin-6), the anti-inflammatory cytokine interleukin-10, and their signaling pathways in PBC, so as to deepen the understanding of the pathogenesis of PBC and explore new treatment methods.
ABSTRACT
Primary biliary cholangitis (PBC) is an autoimmune liver disease characterized by nonsuppurative inflammation of the small- and medium-sized bile ducts in the liver. The pathogenesis of PBC remains unclear, and immunoregulation may play a critical role. As the important components of the immune system, cytokines may be involved in the pathogenesis of PBC. This article reviews related research advances in recent years, including the roles of pro-inflammatory cytokines (interleukin-12, interleukin-17, interleukin-9, interleukin-8, tumor necrosis factor-α, and interleukin-6), the anti-inflammatory cytokine interleukin-10, and their signaling pathways in PBC, so as to deepen the understanding of the pathogenesis of PBC and explore new treatment methods.