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Objective To investigate the inhibition effect of Minocycline on hippocampal microglia in epileptic rats. Methods Forty male SD rats were equally randomized into normal saline control group (NS), penicillin inducement group, Minocycline post-treatment group and Minocycline pre-treatment group (n=10). Rat epilepsy models in the later 3 groups were induced by intraperitoneal injection of penicillin G at a dosage of 740 million to 7.6 million units/kg. The level of hippocampal microglia in rats of the 4 groups on the 1st and 3rd d of inducement was detected by immunofluorescence and the tumor growth factor-α (TNF-α) protein level was detected by Western blotting on the 1st and 3rd d of inducement. Results Seizure could activate microglia. As compared with those in rats of the penicillin inducement group, the activation and hyperplasia of microglia in the hippoeampus in rats of the minoeyeline post- and pre-treatment groups were obviously inhibited on the 1st and 3rd d of inducement (P≤0.05), and the effects were much obvious in the pretreatment group. The level of TNF-α protein in the penicillin inducement group, minoeycline post- and pre-treatment groups was significantly higher than that in the NS group on the 1st and 3rd d of inducement (P≤0.05); as compared with that in the penicillin inducement group, the level of TNF-α protein in the minocycline post- and pre-treatment groups decreased significantly on the 1st and 3rd of inducement (P≤0.05), especially that in the pretreatment group. Conclusion Minocycline can effectively inhibit the activation and hyperplasia of hippocampal microglia and the releasing of inflammatory factor TNF-αt in epileptic rats.
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Objective To investigate the effect of exogenous kallikrein on apoptosis of the neurons aroundthe cerebralinfarctareain rats. Methods Thirty rats wjth cerebral infarction induced by middle cerebral artery occlusion(MCAO)were assigned randomly into 3 groups(n=10),namely the blank control group,saline group,and pAdCMV-HTK group.In the pAdCMV-HTK group,kallikrein gene was delivered into the cerebral ischemie lesion via a replication-defective adenovims using stereotaetic injection technique, and the expression of exogenous kallikrein was detected immunohistoehemically.TUNEL staining was performed to evaluate the neuronal apoptosis around the infarct area,and RT-PCR used to detect the mRNA expressions ofbcl-2,bax and caspase-3 in the brain tissues. Results At 24 h aftertreatment there were some HTK expressed cells found in group C and peal(at 72 h after treatment.While compare with group B and group C,there existed significant difference(112±6.1,68±4.2,59±3.9,P<0.05).At 72 h after treatment,the NSS of group C was significantly lower than that ofgruop B and A(6.70±0.16,8.13±0.16,7.93±0.20,P<0.05);7 days after the treatment,the difference was more significant(5.14±0.18,7.82±0.14,7.91±0.10,P<0.01).Apoptotic cells were mostly seen around the infarct area.The ratsinpAdCMV-HTK group showed significantly reduced number of cells positive for TUNEL staining as compared to those in the saline and blank control groups at 3 days(10.1±0.9,16.7±1.1,and 20.4±0.8,respectively)and 7 days after the treatment(15.2±1.2,33.6±1.3,and 28.8±1.7,respectively)(P<0.05).The mRNA levels ofbc1-2.bax and caspasc-3 were elevated in all the groups at 24 h,peaked at 72 h,and decreased gradually till 7 days alter the treatment.Compared with those in the other two groups，bcl-2 mRNA level in the pAdCMV-HTK group increased slightly P>0.05) while bax and caspase-3 mRNA levels decreased markedly(P<0.05) 72 h and 7 days after the treatment.Conclusion Kallikrein can inhibit neuronal apoptosis around the cerebral infarct and improve the neurological fimction of rats following cerebral infarction probably by reducing the expressions of such apoptotic factors as bax and caspase-3.
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Objective To investigate the effects ofkallikrein gene transfer on microvascularproliferation around the cerebral infarct and on the recovery of regional cerebral blood flow (rCBF)following ischemia/reperfusion injury in rats. Methods The rats with cerebral ischemia/reperfusioninjury induced by middle cerebral artery occlusion (MCAO) were randomly assigned into blank controlgroup, saline group, and pAdCMV-HTK treatment group and received corresponding injections into thetissues around the infarct area. Each group was divided into 3 subgroups (n=10) for observation at 12, 24and 72 h after the treatment. The neurological deficits of the rats before and after the treatment wereevaluated using neurological severity scores (NSS), and the expressions of exogenous human tissuekallikrein (HTK) and vascular endothelial growth factor (VEGF) in the brain tissues were detectedimmunohistochemically. TIC staining was performed to measure the changes in the infarct size.14C-iodoantipyrine tracing technique was used to define the rCBF in the rats. Results Compared tothe blank control group, the cerebral infarct size was significantly reduced in pAdCMV-HTK group 24 hafter the treatment, and was further reduced at 72 h (P<0.05). At 24 h after the treatment, the NSS inpAdCMV-HTK group was significantly lower than that in the blank euntrol and saline groups (P<0.05),and was further reduced at 72 h (P<0.01). After MCAO, the VEGF-positive cells were found mostly inthe cortex and the white matter around the infarct area. The expression of VEGF in pAdCMV-HTK groupwas markedly higher than that in the other two groups at 12, 24, and 72 h after the treatment (P<0.05). Inall the 3 groups, the rCBF around the infarct was slightly decreased as compared to that in thecontralateral hemisphere, pAdCMV-HTK slightly increased the rCBF 12 h after the injection (P>0.05),and significant increase in the rCBF occurred 24 h and 72 h after the injection (P<0.05). ConclusionKallikrein gene transfer following cerebral ischemia/reperfusion injury promotes vascular proliferationaround the infarct and increases the rCBF to reduce the infarct volume and attenuate neurological deficitsin rats.
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<p><b>OBJECTIVE</b>To investigate the incidence, case fatality and risk factors of acute cerebral arterial thrombosis complicated by multiple organ dysfunction syndrome (MODS).</p><p><b>METHODS</b>A retrospective study was conducted in 830 patients with acute cerebral arterial thrombosis, among whom 89 also developed MODS.</p><p><b>RESULTS</b>The incidence of MODS in these patients was 10.7% with case fatality of 58.4%. The presence of concurrent infection and increased number of organ involved both resulted in higher case fatality. The preceding health status, number of failing organs and score of neurologic impairment were the main fetal factors according to logistic regression analysis.</p><p><b>CONCLUSION</b>MODS usually occurs in two weeks after the onset of acute cerebral arterial thrombosis. Prevention of MODS involves rigorous treatment of the compromised organs and comprehensive systemic therapy in addition to the management of the primary diseases.</p>
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Female , Humans , Male , Middle Aged , Cerebral Arterial Diseases , Diagnosis , Epidemiology , Mortality , Intracranial Thrombosis , Diagnosis , Epidemiology , Mortality , Multiple Organ Failure , Diagnosis , Epidemiology , Mortality , Prognosis , Risk FactorsABSTRACT
Objective To investigate the effect of Ulinastatin on the delivery of cytokines in patients with septic shock.Methods It was a prospective and controlled clinical study.Seventy-eight patients with septic shock were randomly divided into control group and treatment group and thirty-nine in every group.Patients in treatment group received Ulinastatin 200 000 units intravenous everyday for 3 days,while those in control group received equal volume of normal saline as placebo.At different time points (at 24 th,48 th,72 th hour after start of treatment),the levels of tumor necrosis factor-alpha (TNF-?),interleukin-1 (IL-1),interleukin-6 (IL-6 ),interleukin-8 (IL-8) and superoxide dismutase (SOD) in serum were assayed.Results In comparison with control group,the levels of TNF-?,IL-1,IL-6,IL- 8 of treatment group decreased markedly (P＜0.05,P＜0.01) at different time points,whereas the level of SOD was higher markedly (P＜0.05,P＜0.01) at various time points.Conclusion Ulinastatin has protective effect on patients with septic shock through decreasing the levels of TNF-?,IL-1,IL-6,IL-8 and increasing in the level of SOD.