1.The analysis of risk factors for the recurrence of senior patients with cerebral infarction
Yuxiang CHEN ; Yulan CHEN ; Lunxue QU ; Rong FEI ; Yong HUANG
Chongqing Medicine 2013;(24):2839-2841
Objective To explore the risk factors for the recurrence of senior patients with cerebral infarction ,and provide refer-ences for its prevention .Methods The 102 elder patients(age>65y) with cerebral infarction were regarded as recurrent group ,and 218 elder cerebral infarction patients without recurrence were considered as primary group .The sex ,age ,body mass index(BMI) , heavy smoking ,drunkenness ,TIA ,location of primary cerebral infarction ,using anti-platelet drugs ,diabetes ,hypertension ,coronary heart disease ,hyperlipidemia ,carotid atherosclerotic plaque ,fibrillation atrial ,chronic obstructive pulmonary diseases (COPD) ,in-creased serum levels of homocysteine(Hcy) ,and high level of C reaction protein(CRP) were analyzed by single and multi factors a-nalysis .Results The single analysis showed the factors including hypertension ,TIA ,carotid atherosclerotic plaque ,heavy smoking , hyperlipidemia ,diabetes ,coronary heart disease ,increased serum levels of homocysteine (Hcy) ,and high level of C reaction protein (CRP) were risk factors for the recurrence of senior patients with cerebral infarction ,but using anti-platelet drugs was the protec-tive factor .Multi-factors analysis showed the factors including coronary heart disease ,hyperlipidemia ,TIA ,diabetes ,carotid athero-sclerotic plaque ,hypertension ,heavy smoking were isolated risk factors but using anti-platelet drugs was the protective factor .Con-clusion There are multitude factors for the recurrence of senior patients with cerebral infarction .We must pain more attention to the factors and decrease their recurrence .
2.Interleukin-10 regulates functions of dendritic cell through autophagy inhibition
Yulan QU ; Jiewen DENG ; Changwen DENG ; Fucan XIA ; Zhenhong GUO ; Chong BAI
Chinese Journal of Immunology 2017;33(3):333-337
Objective:To study the mechanism of interleukin-10(IL-10)inhibiting the function of dendritic cells(DCs).Meth-ods:Cultured C57BL/6 mouse bone marrow-derived DCs were divided into 5 groups:control group,LPS stimulated group,IL-10 treated group,IL-10+Rapamycin treated group and Rapamycin treated group .The regulatory mechanism of IL-10 on dendritic cells were evalua-ted from DCs function ,Flow cytometry was used to analyse the expression of DCs surface co-stimulator CD80 ,CD40 expression ,the abil-ity of uptaking antigen and stimulating T cell to proliferate;ELISA was used to detect the cytokines IL-6 and TNF-α.Western blot was used to analyse the autophagy related protein LC3.Compared the differences between the groups.Results:(1)Compared to LPS stimu-lated group,IL-10 treated group,DCs surface co-stimulator CD40,CD80 were decreased,IL-6 and TNF-αsecretion level and the ability to stimulate T cell to proliferate were decreased ,the ability to capture OVA antigen was increased .Compared to IL-10 treated group ,the DCs surface co-stimulator CD80 was decreased ( P<0.05 ) ,IL-6 and TNF-αsecretion level and the ability to stimulate T cell to prolifer-ate were increased(P<0.0001)in IL-10+rapamycin treated group.In addition,autophagy related proteins LC3Ⅱ/LC3Ⅰwas decreased in IL-10 treated group.Conclusion:IL-10 may regulate functions of DCs through inhibiting the autophagy of DCs .
3.Effects of orexin A on morphine-induced gastrointestinal dysfunction in mice
Junmei ZHANG ; Chuanqi YANG ; Shanshan QU ; Rongrong HUANG ; Shaoli DING ; Kaihua YU ; Yulan LI
Chinese Journal of Anesthesiology 2022;42(11):1324-1328
Objective:To evaluate the effect of orexin A on morphine-induced gastrointestinal dysfunction in mice.Methods:Forty SPF C57B/6 mice, aged 6-8 weeks, half male and half female, weighing 18-22 g, were divided into 5 groups ( n=8 each) using a random number table method: control group (group C), morphine group (group M) and morphine + different doses of orexin A groups (MOH, MOM and MOL groups). Normal saline 8 ml/kg was subcutaneously injected daily in group C, morphine 6 mg/kg was subcutaneously injected daily in the other four groups, and orexin A 75, 50 and 25 μg/kg were subcutaneously injected daily for 10 days at the same time in MOH, MOM and MOL groups.The fetal water content was calculated and averaged daily.After the last administration, the mice were gavaged with black nutrient paste, and the gastric emptying rate and small intestinal propulsion rate were detected 30 min later.Blood samples were collected from the orbit, and the concentration of serum gastrin (GAS) was detected by enzyme-linked immunosorbent assay.The mice were then sacrificed, and colon tissues were removed for determination of c-kit positive cell area (by immunohistochemistry) and expression of c-kit, substance P (SP) and neural nitric oxide synthase (nNOS) in colon tissues (by Western blot). Results:Compared with group C, the rate of fecal water content, gastric emptying rate, small intestinal propulsion rate and serum GAS concentration were significantly decreased, the area of c-kit positive cells was decreased, and the expression of c-kit and SP was down-regulated, and the expression of nNOS was up-regulated in group M ( P<0.05). Compared with group M, the small intestinal propulsive rate and serum GAS concentration were significantly increased, and the area of c-kit positive cells was increased, and the expression of c-kit was up-regulated in group MOH, the rate of fecal water content, gastric emptying rate, small intestinal propulsion rate and serum GAS concentration were significantly increased, the area of c-kit positive cells was increased, and the expression of c-kit and SP was up-regulated, and the expression of nNOS was down-regulated in group MOM, and the serum GAS concentration and c-kit positive cell area were significantly increased in group MOL ( P<0.05). Conclusions:Orexin A 50 μg/kg can effectively alleviate the gastrointestinal dysfunction induced by morphine in mice, and the mechanism may be related to promotion of GAS secretion, interstitial cells of Cajal growth and SP release and inhibition of NO release.