Objective To investigate the effect of acute injury caused by surgery on spatial learning and memory and the underlying mechanism. Methods Ninty-eight healthy SD rats of both sexes weighing 300-350 g were randomly divided into 3 groups: (A) control group received neither anesthesia nor surgery ( n = 14); (B) anesthesia group received intraperitoneal fentanyl 0.2 mg?kg-1 and droperidol 5 mg?kg-1 only ( n = 42) and ( C) splenectomy group received splenectomy under fentanyl and droperidol anesthesia ( n = 42) . Y-maze test was performed to assess the ability of spatial learning and memory in group A and on the 1 st, 3 rd and 7 th day after anesthesia or surgery in group B and C. Seven rats were killed immediately after Y-maze test in group A and on the 1 st, 3 rd and 7 th day after anesthesia (in group B) and surgery (in group C) , and hippocampus was immediately removed for determination of the expression of TNF-? and IL-1? mRNA (RT-PCR) and protein (Western blot). Results The voltage of electric stimulation was significantly higher in group C on the 1st day after surgery than in group B on the 1st day after anesthesia and in group A. The time spent to learn and remember in Y-maze test was significantly longer in group C on the 3 rd than in group B on the 3 rd day and in group A. The expression of TNF-? mRNA and IL-1? mRNA and protein was significantly higher in group C than in group B on the 1st day and in group A.Conclusion Splenectomy can impair the spatial learning ability for a short time after surgery. The increase in the expression of TNF-? mRNA and IL-1? mRNA and protein in hippocampus may play a role in the mechanism.

AIM:?To?investigate?if?alfentanil?protects?the?isolated?rat?heart?against?myocardial?reperfusion?injury?and?if?the?mechanism?of?this?protection?is?mediated?via?opioid?receptors?and?NO-dependent?pathways. METHODS: Langendorff rat hearts were perfused at constant pressure with Kreb-Henseleit(K-H) buffer for 20 min?and?then?were?perfused?with?test?solution:?K-H?buffer?or?K-H?buffer?containing?alfentanil? 50 ?g?L -1,?alfentanil? 100 ?g?L -1, naloxone 200 ?g?L -1, alfentanil 100 ?g?L -1+naloxone 200 ?g?L -1, L-NAME 100 ?mol?L -1 and alfentanil 100 ?g?L -1+L-NAME 100 ?mol?L -1. After 10 min of this, the hearts were subjected to 25 min normothermic( 37 ℃) global ischemia followed by 30 min reperfusion with the same test solution as before. To evaluate myocardial function, LVEDP, LVDP, ?dp/dt max, HR and CF were measured at the 20th, 25 and 30th minute of perfusion and the 1st, 3rd, 5th, 10th, 20th and 30th minute of reperfusion. After experiment, the NOS and ATP content of myocardium were assessed. RESULTS: Before ischemia, alfentanil 100 ?g?L -1 decreased the HR at the 30th minute compared with the 20th minute(P

Aim To investigate whether endogenous hydrogen sulfide participated in the ischemic postconditioning against ischemia/reperfusion injury in the isolated rat hearts.Methods Isolated SD rat hearts were subjected to ischemia by stopping perfusion for 30 min followed by reperfusion for 60 min in Langendorff perfusion system,at the onset of reperfusion,4 cycles of 15 seconds reperfusion followed by 15 seconds ischemia were given for postconditioning.Intraperitoneal injection of L-propargylglycine(PAG,the inhibitor of cystanthionine-?-lysase) half an hour before operation or administration of exogenous hydrogen sulfide donor-NaHS for postconditioning was performed to observe the impact on ischemic postconditioning.The heart rate(HR),left ventricular developed pressure(LVDP),coronary arterial flow(CF)were recorded.The activity of lactate dehydrogenase(LDH)in the coronary effluent fluid,and the activity of CSE and the content of H2S in the isolated rat hearts were measured with colorimetry method.The infarction sizes were measured with TTC dying method.Results In ischemic/reperfusion group,LVDP decreased,the activity of LDH in the coronary effluent fluid and the size of myocardial infarction increased(vs control,P

Aromatic compounds are a class of organic compounds with benzene ring(s). Aromatic compounds are hardly decomposed due to its stable structure and can be accumulated in the food cycle, posing a great threat to the ecological environment and human health. Bacteria have a strong catabolic ability to degrade various refractory organic contaminants (e.g., polycyclic aromatic hydrocarbons, PAHs). The adsorption and transportation are prerequisites for the catabolism of aromatic compounds by bacteria. While remarkable progress has been made in understanding the metabolism of aromatic compounds in bacterial degraders, the systems responsible for the uptake and transport of aromatic compounds are poorly understood. Here we summarize the effect of cell-surface hydrophobicity, biofilm formation, and bacterial chemotaxis on the bacterial adsorption of aromatic compounds. Besides, the effects of outer membrane transport systems (such as FadL family, TonB-dependent receptors, and OmpW family), and inner membrane transport systems (such as major facilitator superfamily (MFS) transporter and ATP-binding cassette (ABC) transporter) involved in the membrane transport of these compounds are summarized. Moreover, the mechanism of transmembrane transport is also discussed. This review may serve as a reference for the prevention and remediation of aromatic pollutants.
Humans ; Adsorption ; Bacteria/metabolism* ; Organic Chemicals ; Biological Transport ; ATP-Binding Cassette Transporters ; Polycyclic Aromatic Hydrocarbons/metabolism*