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Objective@#To evaluate the role of hippocampal mast cells in the early postoperative cognitive impairment in rats.@*Methods@#Eighty male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 4 groups (n=20 each) using a random number table method: normal saline control group (group C), cromolyn injected into lateral cerebral ventricle group (group L), operation group (group O), and cromolyn injected into lateral cerebral ventricle plus operation group (group LO). Cromolyn 2 μl (100 μg/ul) was intracerebroventricularly injected in L and LO groups.The equal volume of normal saline was given instead in C and O groups.Open reduction and internal fixation was performed after tibial fracture was induced 30 min later in O and LO groups.Contextual fear conditioning and Y-maze tests were performed at 1 and 3 days after operation, and the freezing time and the number of learning trails were recorded.The animals were then sacrificed, and hippocampal tissues were obtained for determination of activated mast cell count (by toluidine blue staining) and expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) mRNA (by polymerase chain reaction).@*Results@#Compared with group C, the number of learning trails was significantly increased, and the freezing time was shortened, the number of activated mast cells in hippocampi was increased, and the expression of IL-1β mRNA was up-regulated at 1 and 3 days after operation, and the expression of TNF-α mRNA was up-regulated at 1 day after operation in group O(P<0.05), and no significant change was found in the parameters mentioned above in group L (P>0.05). Compared with group O, the number of learning trails was significantly decreased, and the freezing time was prolonged, the number of activated mast cells in hippocampi was decreased, and the expression of IL-1β mRNA in hippocampi was down-regulated at 1 and 3 days after operation, and the expression of TNF-α mRNA in hippocampi was down-regulated at 1 day after operation in group LO (P<0.05).@*Conclusion@#Activation of hippocampal mast cells can induce central inflammatory responses and is involved in the mechanism of early postoperative cognitive impairment in rats.
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Objective To evaluate the role of hippocampal mast cells in the early postoperative cognitive impairment in rats.Methods Eighty male Sprague-Dawley rats,aged 6-8 weeks,weighing 200-250 g,were divided into 4 groups (n=20 each) using a random number table method:normal saline control group (group C),cromolyn injected into lateral cerebral ventricle group (group L),operation group (group O),and cromolyn injected into lateral cerebral ventricle plus operation group (group LO).Cromolyn 2 μl (100 μg/ul) was intracerebroventricularly injected in L and LO groups.The equal volume of normal saline was given instead in C and O groups.Open reduction and internal fixation was performed after tibial fracture was induced 30 min later in O and LO groups.Contextual fear conditioning and Y-maze tests were performed at 1 and 3 days after operation,and the freezing time and the number of learning trails were recorded.The animals were then sacrificed,and hippocampal tissues were obtained for determination of activated mast cell count (by toluidine blue staining) and expression of tumor necrosis factor-alpha (TNF-α)and interleukin-1beta (IL-1β) mRNA (by polymerase chain reaction).Results Compared with group C,the number of learning trails was significantly increased,and the freezing time was shortened,the number of activated mast cells in hippocampi was increased,and the expression of IL-1β mRNA was up-regulated at 1 and 3 days after operation,and the expression of TNF-α mRNA was up-regulated at 1 day after operation in group O (P＜0.05),and no significant change was found in the parameters mentioned above in group L (P＞0.05).Compared with group O,the number of learning trails was significantly decreased,and the freezing time was prolonged,the number of activated mast cells in hippocampi was decreased,and the expression of IL-1β mRNA in hippocampi was down-regulated at 1 and 3 days after operation,and the expression of TNF-α mRNA in hippocampi was down-regulated at 1 day after operation in group LO (P＜0.05).Conclusion Activation of hippocampal mast cells can induce central inflammatory responses and is involved in the mechanism of early postoperative cognitive impairment in rats.
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Objective: To evaluate the quality consistency of four domestic nifedipine sustained release tablets by dissolution test and virtual bioequivalence study by GastroPlus software.Methods: The dissolution curves of the four preparations were determined with the methods described in Japanese orange book and Chinese Pharmacopeia.The f2 factor of dissolution curves was calculated to compare the similarity.The in vitro dissolution data of the original preparation were combined with GastroPlus software to obtain the simulated in vivo absorption curves which were correlated with the actual concentration-time curves.The suitable dissolution medium was selected to evaluate the quality of domestic nifedipine sustained release tablets according to the better in vivo-in vitro correlation (IVIVC).The simulated in vivo absorption parameters obtained from the dissolution data combined with GastroPlus software were used to conduct the virtual bioequivalence study of domestic nifedipine sustained release tablets compared with the original products.Results: The f2 similar factors of the four domestic nifedipine sustained release tablets compared with the original preparation were all less than 50.Compared with that from the method in Japanese orange book, the correlation between the dissolution profiles in vitro and in vivo of original nifedipine sustained release tablets obtained from the method in Chinese Pharmacopoeia was better.The deviation between the simulated Cmax and AUC0-∞ values of the four test tablets and the measured values of the original preparation was within the range of ±20%.Conclusion: The dissolution curves of the four domestic nifedipine sustained release tablets are not similar to that of the original preparation, however, the four preparations are all bioequivalent to the original preparation according to the simulated absorption parameters based on the dissolution method in Chinese Pharmacopeia and GastroPlus software.
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Objective To investigate the role of A2B adenosine receptor(A2BAR)in 6% HES 130/0.4-induced reduction of pulmonary capillary permeability in a rat model of sepsis.Methods Fifty male SD rats weighing 250-300 g were randomly divided into 5 groups(n = 10 each): group Ⅰ sham operation(group S);group Ⅱ sepsis(group CLP);group Ⅲ ,Ⅳ,Ⅴ low,medium,high dose HES(group H1,2,3).The animals were anesthetized with intraperitoneal pentobarbital sodium 50 mg/kg.Left carotid artery and left femoral vein were cannulated for MAP and HR monitoring and fluid and drug administration.Sepsis was induced by cecal ligation and puncture (CLP).6% HES 130/0.4 7.5,15.0 and 30.0 ml/kg were infused iv over 2 h in group H1,2,3 respectively at 4 h after CLP.The animals were sacrificed at 6 h after CLP.The lungs were isolated for determination of pulmonary capillary permeability(by iv Evans blue injection),the expression of A2BAR and the contents of cAMP,protein kinase A(PKA),TNF-α,IL-6 and IL-10 in the lung tissue.Results CLP significantly increased pulmonary capillary permeability,A2BAR expression and cAMP,IL-6 and TNF-α contents in the lung tissue in group Ⅱ as compared with group S.0.6% HES 130/0.4 significantly reduced pulmonary capillary permeability,increased A2BAR expression,cAMP,PKA and IL-10 and decreased IL-6 and TNF-αcontents in the lung tissue in group H1,2,3 as compared with group CLP.6% HES 130/0.4 decreased pulmonary capillary permeability and up-regulated A2BAR expression in a dose-dependent manner.6% HES 130/0.4 15.0 ml/kg was most effective in increasing cAMP and PKA contents in the lung and depressing inflammatory response.Conclusion 6% HES 130/0.4 decreases pulmonary capillary permeability in a rat model of sepsis by up-regulating A2BAR expression in lung tissue.
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Objective To evaluate the effect of hydrogen sulfide combined with mild hypothermia on cerebral ischemia-reperfusion (I/R) injury in rats. Methods Eighty male SD rats, aged 3 months, weighing 250-300 g, were randomly divided into 5 groups ( n = 16 each): sham operation group (group S), cerebral I/R group,mild hypothermia group (group M), sodium hydrosulfide group (group NaHS) and NaHS + mild hypothermia group (group NM). In group I/R, M, NaHS and NM, cerebral I/R was induced by occlusion of 4 vessels (cauterization of bilateral vertebral arteries and 15 min occlusion of bilateral common carotid arteries) followed by reperfusion. In group NaHS and NM, intraperitoneal NaHS 14 μmol/kg was injected immediately after reperfusion, while the equal volume of normal saline was injected in the other three groups. At the same time, the rectal temperature was reduced to 32-33 ℃ within 15 min, lasting for 6 h, in group M and NM, while it was maintained at 36-37 ℃by physical method in other groups. Twelve rats of each group were sacrificed after 6 h of reperfusion, and then the hippocampus was removed for determination of the content of H2 S by using spectrophotometer and the expression of p-CREB and BDNF mRNA by using Western blot and RT-PCR respectively. Four rats in each group were sacririced after 72 h of reperfusion and then the hippocampus was removed for microscopic examination. Results The cerebral I/R injury was attenuated in group M, NaHS and NM compared with group I/R, with the slightest injury in group NM. The H2S content was significantly higher in group I/R, M, NaHS and NM than in group S, and in group NaHS and NM than in group I/R and M. The expression of p-CREB and BNDF mRNA was significantly higher in group I/R, M, NaHS and NM than in group S, and in group M, NaHS and NM than in group I/R. The BDNF mRNA expression was significantly higher in group NM than in group M and NaHS. There was no significant difference in the H2S content and the expression of p-CREB and BNDF mRNA between group NaHS and M.Conclusion Hydrogen sulfide combined with mild hypothermia can attenuate cerebral I/R injury by up-regulating the expression of p-CREB and BDNF mRNA in hippocampus in rats.
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Objective To investigate the effect of hydrogen-rich saline combined with mild hypothermia on cerebral ischemia-reperfusion (IR) injury in rats. Methods Fifty male SD rats, aged 9-10 weeks, weiging 250-300 g, were randomly divided into 5 groups (n= 10 each): sham operation group (group S), group IR, hygrogen-rich saline group (group H), mild hypothermia group (group M) and hydrogen-rich saline + mild hypothermia group (group HM). In group IR, H, M and HM cerebral IR was induced by 15 min ligation of bilateral carotid artery followed by 6 h reperfusion. In group H and HM intraperitoneal hydrogen-rich saline 5 ml/kg was injected immediately after reperfusion, while the equal volume of normal saline was injected instead of hydrogen-rich saline in the other three groups. At the same time, the rectal temperature was maintained at 37-38 ℃ in group S,IR and M, while it was reduced to 32-34 ℃ by physical method within 15 min, lasting for 6 h, in group M and HM. The animals were sacrificed after 6 h of reperfusion, and then the hippocampus was removed for microscopic examination. The expression of HO-1 and content of MDA and TNF-α were determined by Western blot. Results The cerebral IR injury was attenuated in group H, M and HM compared with group IR, with the slightest injury in group HM. The expression of HO-1 and content of MDA and TNF-α were significantly higher in group IR, H, M and HM than in group S. The expression of HO-1 was significantly higher, while the content of MDA and TNF-α were lower in group H, M and HM than in group IR, and in group HM than in group H and M. There was no significant difference in the expression of HO-1 and content of MDA and TNF-α between group H and M. Conclusion Hydrogen-rich saline combined with mild hypothermia can attenuate cerebral I/R injury in rats via up-regulating the expression of HO-1 and decreasing the content of MDA and TNF-α in hippocampus.
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Objective To investigate the changes in high voltage-activated (HVA) calcium current in dorsal root ganglion (DRG) neurons isolated from rats with neuropathic pain. Methods Pathogen-free male SD rats aged 4-6 weeks weighing 180-220 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 50 mg/kg. Neuropathic pain was induced by ligation of L5 spinal nerve between DRG and sciatic nerve. The nerve was transected distal to the ligature. The animals which showed positive signs of neuropathic pain were decapitated on the 14th postoperative day. L5 and L4 DRGs were isolated and the neurons in the ganglia were enzymatically dissociated (group L5 and L4). The control group received no surgery (group C). The HVA Ca2+ current was recorded using whole-cell patch clamp technique. Results Peak calcium current density was significantly lower in group L5 and L4 than in group C, and was significantly lower in group L5 than in group L4 . Halfactivation value (Va 1/2) was also significantly lower in group L5 than in group C and L4 (P ＜ 0.05). The relative contribution of N-type to the total HVA Ca2+ current was significantly greater in group L5 than in group C and L4(P ＜ 0.05). There was no significant difference in the steady-state inactivation curves among the 3 groups. Conclusion In rats with neuropathic pain, the HVA Ca2+ current in the injured DRG neurons may play a key role in the induction of neuropathic pain.
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The objective was to evaluate the preventive and therapeutic effects of the collagen hydrolysate extracted from Sika deer velvet (CSDV) on osteoporosis rats induced by retinoicacid. Histomorphometric indices and serum biochemical parameters were measured in osteoporosis rats treated with/without antler collagen and in sham-operated rats. Our results were as follows: compared with the osteoporosis group, significant elevation in the levels of bone mineral density (BMD), Ca, P and static histomorphometric indexes and biomechanical properties, but reduction in the level of serum alkaline phosphatase (ALP) were observed in antler collagen-treated groups. However, the above function with the collagenase solution velvet material varied with the different doses. In conclusion, the extracted collagen is found to play a role in the prevention and treatment of osteoporosis rats by retinoic acid.
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Animals , Female , Humans , Male , Rats , Bone Density , Collagen , Metabolism , Therapeutic Uses , Osteoporosis , Osteoporosis, Postmenopausal , Rats, Wistar , Tretinoin , Therapeutic UsesABSTRACT
Objective:To investigate the anti-inflammation,immune regulation and anti-stress effect of cartialgenous collagen zymolyte.Methods:The anti-inflammatory effect was observed by carrageenan-induced foot swelling test,the immune effect was observed by delayed-type hypersensitivity (DTH) induced by 2,4-dinitrochlorobenzene and the anti-stress effect was observed by hypoxia tolerance and fatigue tolerance. Results:The cartialgenous collagen zymolyte can inhibit the carrageenan-induced foot swelling and delayed-type hypersensitivity (DTH) induced by 2,4-dinitrochlorobenzene,and improve the macrophagocyte phagocytosis function,and enhance the body,s non-specific resistance to fatigue.Conclusion:Cartialgenous collagen zymolyte appeared obvious immune regulation,anti-inflammation and anti-stress effect.