ABSTRACT
Postoperative cognitive dysfunction (POCD) is thought to be a mild cognitive disorder.It means that patients without cognitive diseases before surgery suffer from subtle changes in psychomotility,personality,social skills and cognitive function after the surgery.A decline in memory is the core characteristics of these symptoms.POCD is mainly seen in the elderly people following surgery.It can prolong hospital stay,reduce quality of life,increase mortality,and thus aggravate the burden of public health.It is urgent to take precautions to reduce the incidence.The precise mechanism of POCD remains unclear.Previous studies have shown that inflammation plays an important role in it.Sterile surgery can result in peripheral inflammation.Through several pathways,the signals from the peripheral immune response were sent to central system.Due to the individual difference,the degree of the central neuroinflammation was also heterogeneous.Some inflammations may lead to the occurrence of POCD.In order to prevent POCD,we should focus on the anti-inflammatory therapy.
ABSTRACT
<p><b>OBJECTIVE</b>To explore expression changes of myocardial renin angiotensin system induced by prenatal exposure to lipopolysaccharide in offspring rats.</p><p><b>METHODS</b>Twelve pregnant SD rats were randomly divided into three groups: LPS model group: intraperitoneal injection of LPS (0.79 mg/kg) at 8, 10, 12 days of pregnancy; control group: intraperitoneal injection of sterile saline (0.5 ml) at 8, 10, 12 days of pregnancy; LPS + PDTC group: intraperitoneal injection of LPS (0.79 mg/kg) at 8, 10, 12 days of pregnancy plus daily intraperitoneal injection of NF-κB inhibitor -pyrrolidine dithiocarbamate (PDTC, 100 mg/kg) on day 8 to 14 pregnancy day. Protein expression of AngiotensinII(AngII) in heart was detected by immunohistochemistry; myocardial ACE,ACE2 mRNA expression was detected by real-time PCR; protein expression of ACE and ACE2 in heart was detected by Western blot in offspring rats of various groups.</p><p><b>RESULTS</b>Compared with control group (0.07 ± 0.02,0.11 ± 0.01), AngII protein levels (0.14 ± 0.04) were significantly increased at 6 weeks (P < 0.01) and 16 weeks (0.17 ± 0.04, P < 0.05) in offspring rats of LPS model group, which could be significantly attenuated by PDTC intervention (0.10 ± 0.01,0.13 ± 0.03, respectively, all P < 0.05).Similarly, myocardial ACE mRNA expression in 16 weeks offspring rats of LPS model group was significantly upregulated compared with control group (1.10 ± 0.26 vs.0.72 ± 0.22, P < 0.05), which was significantly attenuated by PDTC intervention (0.67 ± 0.01, P < 0.01 vs.LPS group). Myocardial protein expression ACE2 in 16 weeks offspring rats of LPS model group was significantly downregulated compared to control group, which was slightly upregulated by PDTC intervention (P > 0.05).</p><p><b>CONCLUSION</b>Pregnancy exposure to lipopolysaccharide increases myocardial ACE and AngII expression while reduces myocardial ACE2 expression in offspring rats, which might be one of the pathomechanisms of offspring hypertension.</p>
Subject(s)
Animals , Female , Pregnancy , Rats , Angiotensin II , Metabolism , Lipopolysaccharides , Toxicity , Myocardium , Metabolism , Peptidyl-Dipeptidase A , Metabolism , Prenatal Exposure Delayed Effects , Rats, Sprague-Dawley , Renin-Angiotensin SystemABSTRACT
0.05),but was correlated with ?-GT(r=-0.295,P