GM130-silencing may aggravate blood-brain barrier damage and affect microglia polarization by down-regulating PD-L1 expression after experimental intracerebral hemorrhage.

BACKGROUND: In addition to primary injury, secondary injuries related to BBB disruption and immune-inflammatory response also play an important role in intracerebral hemorrhage (ICH). And the Golgi apparatus play an important role in the state of ICH. METHODS: ICH model and GM130-silencing ICH model were established in SD rats. The Garcia score was used to score the neurological defects of the rats. Blood-brain barrier (BBB) integrity were assessed by amount of extravasated Evans blue, and tight junction proteins. The expression of PD-L1 and GM130were detected through Western-blot and the subtype of microglia was showing with Immunofluorescence staining. RESULTS: Compared with the ICH group, GM130-silencing ICH rats got a worsened neurological deficit and enlarged volume of the hematoma. Evan's blue extravasation aggravated as well. The expression of GM130 in peri-hematoma tissue was further decreased, and the morphology and structure of the Golgi apparatus were further damaged. Meanwhile, the GM130 deficit resulted in decreased expression of PD-L1 and more polarization of microglia to the M1 subtype. CONCLUSION: We demonstrate that GM130 could influence the integrity of BBB and plays a role in neuroinflammation via regulation of PD-L1 after ICH. The manipulation of GM130 might be a promising therapeutical target in ICH.

Analysis of antibiotic-induced drug resistance of Salmonella enteritidis and its biofilm formation mechanism.

This research was to explore antibiotic-induced drug resistance of Salmonella enteritidis and its biofilm formation mechanism. Kirby-Bauer (K-B) disk method recommended by Clinical and Laboratory Standards Institute (CLSI) was used to test drug sensitivity of Salmonella enteritidis to 16 kinds of antibiotics including ß-lactams, aminoglycosides, quinolones, sulfonamides, chloramphenicols, and tetracyclines. Polymerase chain reaction (PCR) was performed to detect carrying of drug resistance genes of 29 kinds of antibiotics including ß-lactams, aminoglycosides, quinolones, sulfonamides, chloramphenicols, and tetracyclines of Salmonella enteritidis. The expressions of esp, ebpA, ge1E, and fsrB genes in biofilm group and plankton group were detected when Salmonella was induced, and difference of gene expression was detected by FQ-PCR. The drug resistance rates of Salmonella enteritidis to nalidixic acid, ampicillin, streptomyces, and cefoperazone were high, which were 94.5%, 75%, 67%, and 52%, respectively. 94 strains of Salmonella enteritidis formed 22 kinds of drug resistance spectrum, the strains were generally resistant to 4-5 antibiotics, and some strains formed fixed drug resistance spectrum as follows: AMP-CFP-STR-NA-TE (22.6,21.7%), AMP-STR-NA-TE (17,16%), and AMP-CFP-STR-NA (11.1,10.6%). During biofilm formation, fsr can increase expression of ge1E and decrease expression of esp and ebpA. Consequently, Salmonella enteritidis was generally resistant to nalidixic acid, ampicillin, and streptomycin, and the multidrug resistance was severe. The drug resistance genes sul2, sul3, blaTEM-1-like, tet(A), and tet(G) were highly carried in Salmonella enteritidis. Esp, ebpA, ge1E, and fsrB genes were closely related to biofilm formation of Salmonella enteritidis.

[Risk assessment of Salmonella in broiler chicken].

OBJECTIVE: To assess the risk of foodborne disease caused by Salmonella in broiler chickens from retail to table, and to find effective preventive measures according to the risk assessment results. METHODS: Using dose-response model and Combase database, to evaluate the chicken-Salmonella poisoning risk through the crosscontamination in the kitchen with @ RISK by combining monitoring data of broiler chickens in Heilongjiang Province and related data. RESULTS: According to the results of the quantitative risk assessment, there was a high risk of chicken-Salmonella poisoning because of cross-contamination in the kitchen. Scenario analysis suggested that, if the raw chicken was frozen or refrigerated storage in retail, the average risk of chicken-Salmonella poisoning can be reduced 1/5. CONCLUSION: The risk of Chinese residents suffering from chicken-Salmonella poisoning will be reduced effectively by using cold chain management of raw chicken in retail.

Reduction in ischemic cerebral infarction is mediated through golgi phosphoprotein 3 and Akt/mTOR signaling following salvianolate administration.

Salvianolate has been reported to possess protective properties. However, its specific mechanisms have yet to be identified. Our study aimed to identify the molecular mechanism of antioxidative stress function of salvianolate on rat ischemia and reperfusion brain tissues. Rats were randomly distributed into three experimental groups: sham, model and intervention . All animal neurobehavioral tests were performed at the end of 72-h reperfusion per Longa's method, and rats with a score of 0 (no neurological deficit) or 4 (severe neurological deficit with impaired consciousness) were excluded. Brain slices were obtained after 72 h of reperfusion and stained with triphenyltetrazolium chloride. Western blot analysis and quantitative real-time polymerase chain reaction (qRT-PCR) were used to determine levels of GOLPH3, Akt/p-Akt, and mTOR/p-mTOR expressions in ischemic cortex. Salvianolate (18mg/kg intraperitoneal injection) significantly decreased the neurological deficit scores of rats in groups of 72 h I/R and reduced the number of TUNELpositive cells in the cerebral cortex when given at onset and at 24 and 48 h after reperfusion, leading to decreased cerebral infarction in rats after ischemia/reperfusion injury. Results of Western blot and qRT-PCR showed that salvianolate could significantly upregulate the expression of Golgi phosphoprotein-3 as well as the phosphorylation of Akt and mTOR. Above findings indicate that salvianolate exerts potent and long-term neuroprotective effects in the model of cerebral I/R, and Golgi phosphoprotein-3 and its downstream activation of Akt/mTOR signaling pathway may provide a new insight for the antioxidative effect of salvianolate.

Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model.

Stroke remains a worldwide health problem. Salvianolate exerts a protective effect in various mi-crocirculatory disturbance-related diseases, but studies of the mechanisms underlying its protective action have mainly focused on the myocardium, whereas little research has been carried out in brain tissue following ischemia-reperfusion. We assessed the neuroprotective effects of salvianolate in a rat model of cerebral ischemia-reperfusion injury induced using the suture method. At onset and 24 and 48 hours after reperfusion, rats were intraperitoneally injected with salvianolate (18 mg/kg) or saline. Neurological deficit scores at 72 hours showed that the neurological functions of rats that had received salvianolate were significantly better than those of the rats that had received saline. 2,3,5-Triphenyltetrazolium chloride was used to stain cerebral tissue to determine the extent of the infarct area. A significantly smaller infarct area and a significantly lower number of apoptotic cells were observed after treatment with salvianolate compared with the saline treatment. Expression of heat shock protein 22 and phosphorylated protein kinase B in ischemic brain tissue was significantly greater in rats treated with salvianolate compared with rats treated with saline. Our findings suggest that salvianolate provides neuroprotective effects against cerebral ischemia-reperfusion injury by upregulating heat shock protein 22 and phosphorylated protein kinase B expression.