ABSTRACT
OBJECTIVE: To observe the effect of electroacupuncture (EA) on changes of learning-memory ability, psychomotor coordination and anxiety-like behavior of cerebral hypoxic-ischemia (CHI) young rats, so as to explore its protective effect on neurons under hypoxic-ischemic conditions. METHODS: SD rats (aged 7 days) were randomly divided into sham operation (sham, n=12), model (n=11), and EA groups (n=12). In addition, 6 young rats in each group were used for observing the number of dendritic spines after Golgi staining. The CHI model was established by ligation of the left common carotid artery combined with hypoxia in a closed transparent vessel. EA was applied to "Baihui" (GV 20)and "Dazhui" (GV 14) for 20 min, once every other day, for 28 days. The rats' behavior changes were assessed by using rotarod performance (for psychomotor coordination), elevated plus maze (anxiety-like behavior) tests and Morris water maze (learning-memory ability) tests, separately. RESULTS: After modeling, the average escape latency and average escape distance of location navigation test within 70 seconds were significantly increased (P0.05). The density of dendritic spines was significantly lo-wer in the model group than in the sham group (P <0.05), and notably higher in the EA group than in the model group (P<0.05). CONCLUSION: EA can improve the learning-memory ability of CHI young rats, which may be related to its effect in protecting the dendritic spines of CA 1 region of hippocampus from injury.
ABSTRACT
This study was aimed to explore the mechanism of baicalin on high altitude cerebral hypoxia-ischemia on mice and its influence on related target protein expressions. Morris water maze was used to screen 50 Kunming mice, which were randomly divided into the model group, control group, the low dose (0.05 mg·kg-1), middle dose (0.20 mg·kg-1) and high dose (0.60 mg·kg-1) baicalin group, with 10 rats in each group. The space memory and learning ability of mice were tested. The animal cabin with low oxygen (simulating at 4 000 m altitude) was used to establish the stable high altitude cerebral hypoxia-ischemia mouse model. Changes on SOD content, GSH-PX activities and MDA content in hippocampal tissues of mice were detected. The expressions of different target proteins, including cleaved-caspase 3, P-AKT, GFAP, Bax and Bcl-2 in brain stem of mice were detected by western blot. The results showed that the latent period of the model group was obviously longer than that of the control group (P < 0.05). The latent period of high dose baicalin group was shorter than the model group with significant difference (P< 0.05). Therefore, the best effective dose of baicalin was 0.60 mg·kg-1. Compared with the control group, the content of MDA in the hippocampal tissues of mice in the model group was significantly increased; the SOD and GSH-PX activity were obviously reduced (P < 0.05). Compared with the model group, the SOD and GSH-PX activity were obviously increased in the brain tissues of mice in the high dose baicalin group; and the content of MDA was obviously reduced (P < 0.05). From the level of protein changes, the stripes of cleaved-caspase 3, P-AKT, GFAP protein expressions in the model group were strengthened compared to the control group; the ratio of Bax/Bcl-2 was also obviously increased (P < 0.05). The expression of the baicalin group was lower than that of the model group (P < 0.05). Among them, the expression of the high dose baicalin group was the lowest. It had certain dose-response relationship. It was concluded that baicalin had protective effect on high altitude cerebral hypoxia-ischemia. Its mechanism may be related to its powerful oxidation resistance and its inhibition on expression of different target proteins, including cleaved-caspase 3, P-AKT, GFAP, Bax, Bcl-2 for the change of apoptotic pathway.
ABSTRACT
Objective To investigate the influnce of dexamethasone pretreatment on the expression of ICAM 1 and neutrophil infiltration in brain tissue of hypoxic ischemic neonatal rats Methods Forty eight neonatal rats were made to model with hypoxic ischemic encephalopathy(HIE) The control group and the dexamethasone group were respectively injected intraperitoneally with normal saline 10 ml/kg, dexamethasone 0 1 mg/kg before hypoxia ischemia;all animals were killed 24 hours after hypoxia ischemia Immunocytochemistry was used to determine the absorbency of ICAM 1 The damage grade of neurocytes and leukocyte infiltration were recorded for the histopathological study Results Compared to the control group,the mean absorbency(A) of ICAM 1, the damage grade of neurocytes and neutrophil infiltration of the dexamethasone group were all obviously decreased( P
ABSTRACT
PURPOSE: The selectin family of adhesion molecules plays a role in the initiation of endothelium-leukocyte interaction of inflammation and ischemia-reperfusion. P-selectin, a rapidly expressed endothelial cell adhesion molecule, is essential for both neutrophil rolling after endothelial stimulation and neutrophil transmigration. P-selectins were expressed after brain injury and could play an important role in the pathogenesis of ischemic brain injury in adult animal. However, the mechanisms leading to post-hypoxic-ischemic injury in immature brain are unknown yet. We hypothesize that P-selectin might mediate post-hypoxic-ischemic injury in immature rat brain. We evaluated the expression of mRNA and protein of P-selectin in post-hypoxic-ischemic immature rat brain. METHODS: In isoflurane-anesthetized P7(Postnatal day 7) Sprague-Dawley rats(n=81), the right carotid artery was isolated and coagulated. 1-2 h later animals were exposed to 8% oxygen(balanced with nitrogen) for 2 h in glass chambers, in a warm air incubator (temperature maintained at 36.5 degrees C). Control included carotid artery coagulation alone, hypoxia alone, and normal(neither hypoxia nor coagulation). For RNA extraction, the rats were decapitated at 0, 2, 4, 8, 12, 24 and 48 h after hypoxic-ischemic injury. For Western blot analyses with P-selectin, rats were decapitated at 0, 15, 30 min, 1, 2, 4, 8, 12, 24 and 48 h after hypoxic-ischemic injury. Control or hypoxia alone rats were sacrificed 8 h after the respective intervention. RESULTS: There was no expression of P-selectin mRNA in control groups(carotid artery coagulation alone, hypoxia alone, or normal). P-selectin mRNA expression in the ipsilateral(right) hemisphere reached a peak at 8 h after hypoxia-ischemia and then barely detected after 24 h. Expression of P-selectin protein was not observed in brain tissue of control rats. P-selectin protein was detected as early as 15 min and 30 min at both hemisphere in experimental rats and decreased at 1 h. P-selectin protein increased in right hemisphere at 4 h post-hypoxia-ischemia, peaked at 8 h and no longer detectable at 24 h. CONCLUSION: Hypoxic-ischemic injury leads to P-selectin expression in neonatal rats brain. The temporal profiles of post-hypoxic-ischemic P-selectin mRNA and protein expression are consistent with a role in the evolution of subsequent brain injury.
Subject(s)
Adult , Animals , Humans , Rats , Hypoxia , Arteries , Blotting, Western , Brain Injuries , Brain , Carotid Arteries , Endothelial Cells , Glass , Hypoxia-Ischemia, Brain , Incubators , Inflammation , Neutrophils , P-Selectin , Rats, Sprague-Dawley , RNA , RNA, MessengerABSTRACT
Objective To explore change of RBC[Ca2+]i levels in neonates with hypoxic-ischemic encephalopathy(HIE)and the influence of nimodipine on RBC[Ca2+]i and its clinical significance.Methods Fifty-eight neonates with moderate and severe HIE were randomly divided into 2 groups including routine treatment group(n=28)and nimodipine group(n=30),and 20 healthy full-term neonates were selected as healthy control group.Based on the routine treatment,nimodipine[2 mg,0.5-1.0 ?g/(kg?min)] was given intravenously in the nimodipine group for 7-10 days.Blood samples were collected before and after treatment for 72 hours and 10-14 days,respectively.The levels of RBC[Ca2+]i were measured by Fura-2 pentakis(acetoxymethyl)ester[Fura-2/AM].The results were analyzed by SPSS 10.0 software.Results 1.The levels of RBC[Ca2+]i in neonates with HIE were significantly higher than those in healthy control group[(2.83?0.36)mmol/L vs(2.15?0.18)mmol/L,P