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Objective To evaluate the relationship between sevoflurane-induced cognitive impairment and α1B adrenoceptors (ADRA1B) and ADRA1D in the cerebral cortex of rats.Methods Forty-eight SPF adult Sprague-Dawley rats (half male,half female),weighing 220-260 g,were divided into control group (C group,n =24) and sevoflurane group (S group,n =24) using a random number table method.Group C and group S inhaled air and 3％ sevoflurane,respectively,for 5 h.Eight rats in each group were sacrificed immediately after anesthesia,and the cerebral cortex was removed.Eight rats in each group were selected on days 1 and 7 after anesthesia and underwent Barnes maze test.The rats were then sacrificed,and the cerebral cortex was removed.The expression of ADRA1B and ADRA1D protein and mRNA in cerebral cortex tissues was detected by Western blot and fluorescent quantitative real-time polymerase chain reaction,respectively.Results Compared with group C,the number of entering incorrect holes was significantly increased at 1 and 7 days after anesthesia,the latency and total distance to enter the target hole were prolonged,and the expression of ADRA1B and ADRA1D protein and mRNA in cerebral cortex was down-regulated immediately after anesthesia and at 1 and 7 days after anesthesia in group S (P＜0.05).Conclusion The mechanism underlying sevoflurane-induced cognitive impairment may be related to the down-regulated expression of ADRA1B and ADRA1D in cerebral cortex of rats.
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Objective To evaluate the relationship between sevoflurane-induced cognitive decline and α1A norepinephrine receptor (ADRA1A) in the cerebral cortex of rats.Methods Forty-eight cleangrade healthy adult Sprague-Dawley rats (24 male,24 female),weighing 220-260 g,aged 3-4 months old,were divided into 2 groups (n =24 each) using a random number table method:control group (group C) and sevoflurane group (S group).Group S inhaled 3％ sevoflurane for 5 h.Rats underwent the Barnes maze test on days 1 and 7 after anesthesia.Rats were sacrificed immediately after anesthesia and on days 1 and 7 after anesthesia,and the cerebral cortex was removed for determination of the expression of ADRA1A protein and mRNA (by Western blot or fluorescent quantitative real-time polymerase chain reaction).Results Compared with group C,the number of entering incorrect holes was significantly increased,and the latency of entering the target hole and the distance were prolonged,and the expression of ADRA1A protein and mRNA in cerebral cortex was down-regulated at each time point in group S (P＜0.05).Conclusion The mechanism of sevoflurane-induced cognitive decline is related to down-regulated expression of ADRA1A in the cerebral cortex of rats.
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Objective To investigate the wake-promoting action of median nerve electrical stimulation(MNES) in coma rats induced by traumatic brain injury(TBI) and its influence on the expression of α1-adrenergic receptor(α1 R) in the prefrontal contex (PFC).Methods Seventy-two healthy Sprague Dawley(SD) rats were randomly divided into the control group,sham-stimulated group(TBI),stimulated group (TBI+ MNES) and antagonist group(TBI+ OX1R antagonist +MNES).The control group had no any treatment.The TBI coma rat models were prepared in the other 3 groups.The sham stimulated group had no treatment.The antagonist group was injected with orexin receptor-l(OX1R) antagonist SB334867 into lateral ventricle,and both the antagonist group and stimulated group received MNES treatment.Then the behavior changes of rats in each group were observed and the α1 R expression level in PFC was detected by using the immunohistochemistry technique.Results Thirteen rats in the stimulated group and 8 rats in the antagonist group revived,while only 4 rats in the TBI group.The α1R levels from low to high were the blank control group,sham-stimulated group,antagonist group and stimulated group,showing the increasing trend,and the difference was statistically significant(P＜0.05).Conclusion MNES can improve the rat consciousness level after TBI coma,and its mechanism may be related with up-regulating the α1 R expression level in PFC area,moreover Orexin-A participates in this regulation process.
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PURPOSE: Benign prostatic hyperplasia (BPH) is the most common prostate problem in older men. The present study aimed to investigate the inhibitory effect of Panax ginseng C.A. Meyer (P. ginseng) on a rat model of testosterone-induced BPH. METHODS: The rats were divided into 3 groups (each group, n=10): control, testosterone-induced BPH (20 mg/kg, subcutaneous injection), and P. ginseng (200 mg/kg, orally) groups. After 4 weeks, all animals were sacrificed to examine the blood biochemical profiles, prostate volume, weight, histopathological changes, alpha-1D adrenergic receptor (Adra1d) mRNA expression, and epidermal growth factor receptor (EGFR) and B-cell CLL/lymphoma 2 (BCL2) protein expression. RESULTS: The group treated with P. ginseng showed significantly lesser prostate size and weight than the testosterone-induced BPH group. In addition, P. ginseng decreased the mRNA expression of Adra1d as well as the expression of EGFR and BCL2 in prostate tissue. CONCLUSIONS: These results suggest that P. ginseng may inhibit the alpha-1-adrenergic receptor to suppress the development of BPH.
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Animals , Humans , Male , Rats , B-Lymphocytes , Models, Animal , Panax , Prostate , Prostatic Hyperplasia , ErbB Receptors , Receptors, Adrenergic, alpha-1 , RNA, Messenger , TestosteroneABSTRACT
Objective To explore the role of the autoantibodies against ?_1 and ?_1-adrenergic receptor(?_1-receptor)in the development of hypertension with renal failure.Methods The epitopes of the second extracellular loop of ?_1-receptor(197-222) and ?_1-receptor(192-218) were synthesized and used respectively to screen sera autoantibodies in patients with hypertension and renal failure(n=61),hypertension without renal failure(n=60) and healthy blood donors(n=40,control) by ELISA.Results The positive rates of the autoantibodies against ?_1-receptor(62.3%)and ?_1 receptor(50.8%) in patients with hypertension with renal failure were higher than those of patients with hypertension without renal failure(13.3% and10.0%)(P
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Objective To investigate the effects of antioxidant on the gene expression of ?1-adrenergic receptors (AR) during endotoxic shock. Methods Forty male SD rats weighing 200-250 g were anesthetized with intraperitoneal (i.p.) pentobarbital. The animals kept spontaneous breathing. Femoral artery and vein were cannulated for BP monitoring and drug administration. The animals were randomly divided into 5 groups ( n = 8 each) : (1) control group; (2) LPS group received IPS 15 mg?kg-1 i.v. ; (3) LPS + propofol group received at 1h after LPS a bolus of propofol 10mg?kg-1 i.v. followed by continuous infusion of propofol at 10 mg?kg-1?h-1; (4) LPS + uric acid (UA) group received uric acid 200 mg i.p. 1 h after LPS and (5) LPS + melatonin (MLT) group received MLT 10 mg?kg-1 i.p. 1h after LPS. The animals were killed at 6 h after LPS. Total RNA was extracted from the heart, aorta, vein, lung, liver and kidney. ?1A-,?1B-,?1D- AR mRNA and ?-actin mRNA were measured using reverse transcription polymerase chain reaction (RT-PCR) .Results The expression of ?1A-AR and ?1B-AR mRNA in all the organs and the ?1D-AR mRNA expression in aorta, liver, lung and kidney were strongly down-regulated in LPS group. In group 3 (LPS + propofol) the expression of ?1A-AR mRNA in the lung and kidney, the ?1B-AR mRNA expression in all of the organs and ?1D-AR mRNA expression in aorta, liver, lung and kidney were significantly increased as compared with LPS group. There was no significant difference in ?1-AR mRNA expression between LPS group and LPS + MLT group. The expression of ?1A-AR mRNA in kidney, the ?1B-AR mRNA expression in all of the organs except the lung and the ?1D-AR mRNA expression in aorta, liver, lung and kidney were significantly higher in LPS + UA group than in LPS group. Conclusion Circulatory failure induced by endotoxic shock is related to the down-regulation of ?1-AR gene expression. The therapeutic effects of antioxidant on the endotoxic shock is partly due to up-regulation of ?1-AR gene expression.
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Objective To evaluate the changes in peripheral?1-adrenergic receptor sensitivity in a rat model of chronic high spinal cord injury (SCI)Methods Thirty male 18-week-old Wistar rats weighing 290-310g were randomly divided into 2 groups: SCI group (n=24) and control group (C n=6) . The animals were anesthetized with intraperitoneal 2 % pentobartital 50 mg?kg-1 and subjected to spinal cord injury (SCI) at T4 according to modified Allen's method. Successful high SCI was confirmed by bilateral hindlimb flaccid paralysis. Three weeks after SCI the animals were further divided into 4 subgroups (n=6) receiving 4 different doses of phenylephrine 1, 2, 3 and 4 ?g?kg-1 i.v. Femoral artery was connulated for BP (SBP and DBP) and HR monitoring. HR and SBP and DBP were recorded before and after i.v. phenylephrine injection. In control group phenylephrine (PE) 1,2,3 and 4 ?g?kg-1 were injected i.v. successively at an 1h interval. % changes in HR, SBP and DBP were calculated: % change = (post-injection value- baseline value) / baseline value. Results The animals lost weight and HR was significantly slower and SBP and DBP were significantly lower 3 weeks after SCI as compared with control group. In both group C and SCI, HR was significantly decreased and SBP and DBP were significantly increased after i.v. PE injection as compared to the baseline value before PE. The % changes in HR, SBP and DBP were significantly greater in group SCI than in group C. Conclusion In a rat model of chronic high SCI, peripheral?1-adrenergic receptor sensitivity is significantly increased 3 weeks after high SCI.
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Objective To investigate the effect of nitrotyrosine (3-NT) on the expression of ?1D adrenoceptor (?1D-AR) mRNA in cultured vascular smooth muscle cells (SMCS) .Methods SMCS were obtained from the tunica media of thoracic aorta of 1 month old SD rats and cultured in DMEM medium. The experiment consisted of two parts. In part Ⅰ SMCS were incubated with 0,1, 10, 100 or 200 ?mol?L-1 3-NT for 24 h and in part Ⅱ SMCS were incubated with 100 ?mol?L-1 3-NT forO,12, 24, 48 or 72 h. The total RNA was isolated by using Trizol reagent. The expression of ?1D-AR mRNA was determined by RT-PCR and agarose gel electrophoresis. Results In part I incubation with 1 and 10 ?mol?L- 3-NT for 24 h had no significant effect on the expression of ?1D-AR mRNA while incubation with 100 or 200 ?mol?L-1 3-NT for 24 h decreased the expression of ?1D-AR mRNA compared with 0?mol?L-1 3-NT (P
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Changes of pulmonary ?_1-and ?-adrenergic receptor (?_1-AR and ?-AR)during endotoxin-induced acute lung injury in rates were oberved to find out the rela-tionship between them and the mechanism of change. Results showed that there was amarked decrease of B_max of both ?_1-AR and ?-AR by 35% and 43% respectively, dur-ing acute lung injury. The down regulation of ?-AR might be one of causes of acutelung injury while that of ?_1-AR seems to be a protective response. Active oxygen playedan important role in endotoxin-induced down regulation of AR in the rat lungs. The increa-sed level of norepinephrine and epinephrine was not the main factor that initiate the downregulation of AR. Intravenous injection of tumor necrosis factor (5?10~6U/kg ) exerts noiafluence on the changes of pulmonary AR in rats.
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AIM: To study the mechanism for biological effect of ? 1-adrenoceptors by inves tigating the molecular mechanism involving in the apoptotic processi on in myocardium. METHODS: The expressions of Bcl-2, Bax, cytochrome C, caspase-3 were determined by means of immunohistochemistry and molecular technique. RESULTS: Bcl-2 was increased but apoptosis, Bax, cytochrome C, caspase-3 were decreased when phenylephrine was used before ischemia. CONCLUSION: ? 1 -adrenoceptors may influence the expression of Bcl-2 ,change the permeabil ity of mitochondrion and adjust the expression of apoptotic protein to control apoptosis.