1.Neuronal protection of progesterone against ischemic brain injury and underlying molecular mechanisms
Yanying ZENG ; Wenhong ZHI ; Xinsheng DING ; Zheng WANG ; Weixian CHEN
Chinese Journal of Neurology 2013;(6):387-391
Objective To investigate the effect of progesterone pretreatment of focal cerebral ischemic and reperfusion injury (fCIRI) and underlying molecular mechanisms.Methods A single intraperitoneal injection of progesterone (8 mg/kg) given 1 h,48 h and 96 h before fCIRI was established in male Sprague-Dawley rats.The number of survival of neurons in hippocampal CA1 region of the ischemiaside,as well as spatial memory function,was detected on days 3-8 after fCIRI.Extracellular-signalregulated kinase 1/2 phosphorylation (p-ERK1/2) and nuclear translocation of p-ERK1/2 in hippocampal CA1 region were examined using western blot.Results The number of survival of neuronal cells was significantly increased in ischemic groups treated with progesterone at 1 h and 48 h pre-fCIRI (164.3 ± 11.0,218.5 ± 9.1 and 142.7 ± 12.1,F =29.4,P < 0.01) compared with fCIRI group treated with vehicle.Likewise,the escape-latency to reach the hidden-platform recorded in day 5 of Morris water maze test was reduced markedly in fCIRI-treatment groups compared with the vehicle group(10.3 ± 11.1,19.2 ±9.6 and 32.4 ± 14.3 ;F =35.8,P <0.01).The level of p-ERK1/2 was elevated notably during 24 h to 48 h postprogesterone by western blot,while restored to the baseline at 96 h post-progesterone.Improved nuclear translocation of p-ERK1/2 was observed from 2 h to 48 h post-progesterone.The progesterone receptor antagonist RU486 blocked the exaltation of either intracellular level or nuclear translocation of p-ERK1/2,which was induced by progesterone.Conclusions The pretreatment with progesterone exerts a neuroprotective effect against the ischemia-induced neuronal death and ameliorates the deficits in spatial memory through enhancing the activation of ERK1/2.The neuroprotection derived from pretreatment with progesterone achieves a time window of not less than 48 h,which is progesterone receptor-mediated ERK1/2 signaling pathway-dependent.
2.Protective effects of sulforaphen on neuronal apoptosis after focal cerebral ischemia reperfusion injury in rats
Weixian ZENG ; Daqing CHEN ; Yuqiang GONG ; Laifang SUN ; Zhongqiu LU
Chinese Journal of Emergency Medicine 2013;22(12):1346-1351
Objective To investigate the protective effects of sulforaphen (SFN) on focal cerebral ischemia/reperfusion injuy (IRI) in rats in order to explore the mechanisms.Methods Twenty-four male SD rats were randomly (random number) divided into Sham-operated group (A group,n =8),IRI group (B group,n =12),sulforaphen group (C group,n =8).SD rats were made to be transient focal cerebral IRI models.SFN 5 mg/kg was injected intraperitoneally to rats 15 minutes after IRI in C group,and rats of group A and group B received equal volume PBS instead.Infarct volume was measured by TTC staining and morphologic changes were observed with HE staining.Neuronal cell apoptosis index was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) assay.Rats were sacrificed at 24 h after IRI.The protein levels of NF-κB p65 and iNOS were detected by using western bloting and the mRNA expressions of NF-κB p65 and iNOS were detected by using RT-PCR.Results Compared with the group B,infarct volume was significantly smaller in group C,the number of neuronal cell apoptosis in brain tissue were decreased significantly in group C [(96.34 ±3.72) vs.(124.65 ±3.85),P < 0.01],the levels of NF-κB and iNOS in brain tissue of rats were decreased in the SFN group (P < 0.01).SFN reduced neuronal cell apoptosis,injury,and infarct volume [(0.26 ± 0.018) vs.(0.43 ±0.031),P <0.01].The mRNA expression and protein level of NF-κBp65 were decreased in the group C.And the mRNA expression and protein level of induced nitric oxide synthase (iNOS) in IRI affected brain tissue were decreased in the group C [(0.67 ± 0.042) vs.(0.56 ± 0.032),P < 0.01].Conclusions SFN might decrease the neuronal cell apoptosis caused by ischemia/repeffusion injury,and this protective effect is mediated by decreasing the level of NF-κB and iNOS.
4.Digestive system manifestations in patients with severe acute respiratory syndrome.
Jun ZHAN ; Weixian CHEN ; Chuqiang LI ; Wei WU ; Jianjun LI ; Shanping JIANG ; Jingfeng WANG ; Zhiyong ZENG ; Zitong HUANG ; Hongzhang HUANG
Chinese Medical Journal 2003;116(8):1265-1266
OBJECTIVETo explore digestive system manifestations in patients with severe acute respiratory syndrome (SARS).
METHODThe clinical data of 96 cases with SARS admitted into our hospital from February 6, 2003 to March 28, 2003 were retrospectively analyzed.
RESULTSAmong the 96 cases, 26 cases (27%) had diarrhea, 17 (18%) had nausea, 6 (6%) had vomiting, 16 (17%) had bellyache, and 8 (8%) had ALT elevation.
CONCLUSIONSPatients with SARS may have digestive system manifestations; diarrhea is the most common symptom.
Adolescent ; Adult ; Diarrhea ; etiology ; Digestive System Diseases ; etiology ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Severe Acute Respiratory Syndrome ; complications