首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献，搜索用时 15 毫秒
1.
AIM: To explore the protective effect of panaxadiols (PDS) on brain injury induced by endotoxin and its mechanism. METHODS: Rats were divided into control,LPS,LPS+dexamethasone (DEX) and LPS+PDS group, respectively. NOS activity, NO content and phosphorylated p38 expression in brain cortex were assayed 4 h after intravenous injection of LPS. RESULTS: NOS activity, NO content and phosphorylated p38 expression in brain cortex in LPS group were obviously higher than those in LPS group. NOS activity, NO content and phosphorylated p38 expression in brain cortex in LPS+DEX and LPS +PDS groups were obviously lower than those in LPS group. CONCLUSION: The protective effects of PDS against brain injury induced endotoxin may be related to decreasing NOS activity, NO content in the brain tissue, and this process is involved in p38MAPKs signal transduction.  相似文献   

2.
AIM: To explore the molecular mechanism of panaxadiol saponin (PDS) by observing Toll like receptor (TLR) 2 and TLR9 mRNA expression induced by lipopolysaccharide (LPS).METHODS: Rats were divided into LPS, LPS+PDSL, LPS+PDSM and control group, respectively. Nitric oxide synthase (NOS) activity, nitric oxide (NO) content, LPO content, SOD activity and TLR2 and TLR9 mRNA expression were assayed 4 h after intravenous injection of LPS. RESULTS: NOS activity, NO content, LPO content of LPS+PDSL group and LPS+PDSM group were significantly lower than those in LPS group. TLR2 mRNA expression in the liver tissue of LPS+PDSL group and LPS+PDSM group was decreased compared with LPS group.CONCLUSION: PDS has a protective effect on liver tissues by triggering the down-regulation of TLR2 expression, reducing NOS activity, and NO content.  相似文献   

3.
李娟  周健民 《园艺学报》2006,33(4):730-733
以番茄(Lycopersicon esculentumMill.)‘合作906’为材料进行溶液培养试验,设2个因子:CO2和营养液浓度;CO2浓度设正常(360μL/L)和倍增(720μL/L)2个水平;营养液浓度设基本营养液(日本山崎番茄营养液),微量元素采用阿农营养液配方的1/2、1/4、1/8、1/164个水平,完全试验方案8个处理,3次重复。pH为6·0±0·2,3d更换1次营养液。移植到1·2L盆(2株/盒)中,植株在CO2生长箱(VS-3DMC)中培养,全天施放CO2,白天25℃,晚上15℃,光照为14h/d,光照强度11000lx,相对湿度60%。46d时收获,根、茎、叶经蒸馏水冲洗吸干水分后,放入纸袋105℃杀青,75…  相似文献   

4.
AIM：To investigate whether the panaxadiol saponins (PDS) and dexamethasone (DEX) have similar effects on lipopolysaccharide (LPS)-induced acute kidney injury (AKI). METHODS：C57BL/6 mice were randomly divided into 4 groups: the control mice received intraperitoneal injection of normal saline; in LPS group, the mice were subjected to intraperitoneal injection of LPS (10 mg/kg); in PDS + LPS group and DEX + LPS group, the mice were injected intraperitoneally with PDS (25.0 mg/kg) and DEX(2.5 mg/kg) 1 h before LPS injection, respectively. The blood was collected from the hearts, and the kidneys were collected for the biochemical and Western blotting analysis 12 h after LPS injection. RESULTS：LPS induced AKI, evidenced by markedly increased blood urea nitrogen (BUN) and creatinine (CREA) contents compared with control group (P<0.01). However, serum contents of CREA and BUN obviously reduced in PDS + LPS group and DEX + LPS groups compared with LPS group (P<0.05). Both PDS and DEX decreased the production of TNF-α and IL-6 by inhibiting renal NF-κB signaling activation. PDS and DEX also down-regulated the expression of inducible nitric oxide synthase, up-regulated the expression of manganese superoxide dismutase and reduced oxidative stress in the kidneys of LPS-challenged mice. In addition, treatment with PDS and DEX significantly increased the nuclear glucocorticoid receptor in the kidneys of LPS-treated mice. CONCLUSION：PDS and DEX have inhibitory effects on LPS-induced AKI mice. However, it is unclear whether PDS reduces LPS-induced AKI via direct action on glucocorticoid receptor.  相似文献   

5.
AIM:To explore the molecular mechanism of brain tissue injury induced by lipopolysaccharide (LPS),the effects of panaxadiol (PDS) on the expression of nuclear factor kappa B (NF-κB) in cerebral cortex of rat with LPS shock were studied. METHODS:Rats were randomly divided into LPS roup,LPS+dexamethasone group,LPS+PDS group and control group. The DNA binding activity and protein expression of NF-κB were observed. These indices were assayed at 1 h and 4 h after intravenous injection of LPS (4 mg·kg-1). RESULTS:EMSA showed that PDS inhibited NF-κB DNA-binding activity in nuclear extracts at both 1 h and 4 h after LPS injection,compared with the LPS group (P<0.01). Western blotting showed that PDS down-regulated the expression of p65 and p50 protein in the nuclear extracts compared with the LPS group. However,the expression of p65 and p50 protein from cytosolic extracts did not show any significant change. CONCLUSION:PDS may alleviate brain injury by inhibiting NF-κB activation.  相似文献   

6.
AIM: To investigate the effect of H2S on pulmonary artery hypertension during acute lung injury induced by LPS and the interaction between the systems of hydrogen sulfide (H2S)/cystathionine-β-lyase (CSE) and nitric oxide (NO)/nitric oxide synthase (NOS) in this process. METHODS: Seventy-two adult male rats were randomly divided into four groups: control group, LPS group, LPS+L-NAME group and LPS+propargylglycine (PPG) group. Mean pulmonary artery pressure (mPAP) of each rat was examined at 2 h, 4 h, 6 h and 8 h after treatment. H2S and NO contents in plasma, NO content, iNOS, cNOS and CSE activity in lung were measured at 4 h or 8 h after treatment, respectively. Expression of iNOS in lung tissue was also detected by immunohistochemistry technique, and the injury of lung was evaluated with morphological changes under microscope. RESULTS: LPS could induce severe lung injury, and mPAP, NO content, iNOS activity and its protein expression in LPS group significantly increased, but cNOS activity, H2S content and CSE activity decreased compared with those of control group. Administration of L-NAME before LPS could attenuate the changes induced by LPS. Pre-administration of PPG, a CSE inhibitor, exacerbated the injury by LPS, but there was no prominent variation in cNOS activity. CONCLUSION: Reduced endogenous H2S could increase pulmonary artery hypertension during acute lung injury induced by LPS. There is a negative effect between H2S/CSE system and NO/NOS system in this process.  相似文献   

7.
AIM：To investigate the alteration of aquaporin 1 (AQP1) expression in lung tissues in endotoxic shock rats and the effect of panaxadiols.METHODS：The histological changes were examined by HE staining.The expression of AQP1 was analyzed by immunohistochemical staining and Western blotting.RESULTS：(1) Significant inflammatory changes in pulmonary interstitial in rats of LPS group were observed.However,in dexamethasone (DEX) treatment group and panaxadiols (PDS) treatment group,the pulmonary pathologic changes were much slighter.(2) Positive AQP expression in the endothelium of capillary vessels on the wall of alveolus were seen in control (CTR) group,while merely very weak expression in LPS group was detected.The positive staining in PDS groups and DEX group were significantly stronger than that in LPS group,and close to CTR group.(3) The results of Western blotting showed that the quantity of AQP1 expression in LPS group was significantly lower than that in other groups,also the expression in PDS groups and DEX group was slightly lower than that in control group.CONCLUSION：LPS inhibits the expression of AQP1,while PDS increases the strength of AQP1 expression in lungs of endotoxic shock rats.  相似文献   

8.
AIM: To investigate the effects of nitric oxide (NO) and NO synthase (NOS) inhibitor NG-nitro-L arginine (L-NA) on LPS induced-lung injury in rats. METHODS: Forty healthy male SD rats, weighing 300±20 g, were used. The animals were anesthetized with 20% urethane 1 g·kg-1. Common carotid artery (CAA) and jugular vein were exposed through a median incision in the neck. Mean arterial pressure (MAP) was measured through a pressure transducer connected with intubation of CAA. The animals were randomly divided into five groups: group 1: control; group 2: LPS (5 mg·kg-1, iv); group 3: high dose L-NA (20 mg·kg-1 intraperitoneal injection, ip); gropu 4: middle dose L-NA (10 mg·kg-1, ip); group 5: low dose L-NA (5 mg·kg-1, ip). Group1 : 0.9% saline solution was given and the animals were killed 6 h after the saline solution. Gruop 2: saline solution was given 3 h after LPS and the animals were killed 3 h after administration. Group 3, 4 and 5: L-NA was given 3 h after LPS iv and the animals were killed 3 h after administration, respectively. The pulmonary was removed immediately. The pulmonary coefficient and water content in pulmonary tissue were calculated (%). The NO2-/NO3- content in plasma, MDA content and NOS, SOD activity in the pulmonary tissue were measured. RESULTS: L-NA significantly decreased pulmonary coefficient and water content in pulmonary tissue and ameliorated LPS induced lung injury. The effect in high dose group was better than that in low dose group. L-NA significantly decreased NO2-/NO3- content in plasm, decreased MDA content and inhibited NOS activity and enhanced SOD activity in the pulmonary tissue. CONCLUSION: It may be concluded that L-NA has a beneficial effect on lung injury induced by LPS.  相似文献   

9.
AIM:To explore the relationship between renin-angiotensin system (RAS) and acute lung injury (ALI) in rats, and the effect of dexamethasone (DEX) on RAS was observed.METHODS: The rat model of ALI was induced by hemorrhagic shock and LPS administered intraperitoneally. The changes of MAP and the effects of DEX on MAP were observed. The mRNA expressions of ACE, AGT, AT1 and AT2 in lung tissue were assayed by RT-PCR. The changes of Ang I and Ang II in the serum and the effects of DEX on them were observed.RESULTS: The increasing of MAP was statistically obvious. MAP in hemorrhagic shock+LPS (HL) group recovered more slowly than that in HL+DEX(HLD) group. ACE, AGT, AT1 and AT2 mRNA expressions in HL group were increased, and higher than those in HLD group. The change of Ang II in serum in HL group was obviously higher than that in HLD group, while that of Ang I was not obvious.CONCLUSION:ALI activates RAS in rat lung, and promotes the production of Ang II then aggravates the injury of lung through increasing the expression of ACE and AGT. DEX decreases expression of Ang II.  相似文献   

10.
AIM: To investigate the effects of external counterpulsation (ECP) on nitric oxide (NO) and nitric oxide synthase (NOS) and the expression of NOS gene in myocardial infarction canines. METHODS: Nineteen healthy dogs were randomly divided into three groups ie. controls, ischemia group, ischemia and ECP group. Serum NO concentrations and myocardium NO levels and NOS specific activity were determined by modified nitrate reductase method. The protein synthesis of sub-type NOS including inducible NOS (iNOS) and endothelial NOS (eNOS) of myocardial tissue were also determined by immunohistochemical method. The constitutive NOS (cNOS) mRNA was measured via in situ hybridization. RESULTS: 120 and 180 minutes after the ligating of LAD, serum NO concentration in ECP groups were higher than those in ischemic groups (P＜0.05). The NO levels and NOS specific activity in myocardium of ischemic dogs were lower than those in controls and ECP group (P＜0.05). Protein synthesis of iNOS increased and that of eNOS decreased in ischemic myocardium. But ECP could control the protein synthesis of iNOS, and increase that of eNOS. Further studies showed that the expression of cNOS mRNA decreased in ischemic myocardial tissue, ECP might promote the expression of it and regulate NOS in the gene level. CONCLUSION: The results suggested that it was one of the most important mechanisms through raising the NO levels to protect ischemic myocardium in ECP.  相似文献   

11.
AIM: To explore the role of NO in the induction of brain ischemic tolerance (BIT) by observing changes of NOS activity and NO2-/NO3- content following a transient cerebral ischemia. METHODS: The rat 4-vessel occluding brain ischemic model was used. 140 male Wistar rats were divided into sham, cerebral ischemic preconditioning (CIP), ischemic insult and CIP+ischemic insult groups. An occlusion of the 4 vessels for 3 min was normally used as CIP, and a relative long one for 10 min was used as ischemic insult. When CIP was followed by ischemic insult, the interval between them was 3 d. The CA1 region of the hippocampus of rats was dissected out at 0 h, 2 h, 16 h, 24 h, 36 h, 72 h and 7 d after the last time of ischemia to assay its NOS activity and NO2-/NO3- content. RESULTS: The NOS activity and NO2-/NO3- content began to increase at 16 h, peaked at 24 h and decreased to basal level at 36 h of reperfusion after CIP. The duration of the up-regulation of NOS activity and NO2-/NO3- content was much shorter than that of BIT, which usually takes place 1-7 d after CIP. The pattern of upregulation of the NOS activity and NO2-/NO3- content was similar to the CIP group, but the maximum (24 h) was much more than that in CIP group (P<0.05). In the CIP＋ischemic insult group, the NOS activity and NO2-/NO3- content increased at 2 h of reperfusion, but the maximum (24 h) were much lower than that in ischemic insult group (P<0.05). CONCLUSION: A moderate increase in NOS activity and NO production after CIP might participate in the induction of BIT by triggering a series of cellular signal transduction. In addition, inhibiting effect of CIP on over-production of NO caused by ischemic insult might be another way to induce BIT.  相似文献   

12.
AIM:To investigate the effects of external counterpulsation(ECP)on nitric oxide(NO)and nitric oxide synthase(NOS)and the expression of NOS gene in myocardial infarction canines.METHODS:Nineteen healthy dogs were randomly divided into three groups ie.controls, ischemia group, ischemia and ECP group.Serum NO concentrations and myocardium NO levels and NOS specific activity were determined by modified nitrate reductase method.T he protein synthesis of sub-type NOS including inducible NOS(iNOS)and endothelial NOS(eNOS)of myocardial tissue were also determined by immunohistochemical method.The constitutive NOS(cNOS)mRNA was measured via in situ hybridization.RESULTS:120 and 180 minutes after the ligat ing of LAD, serum NO concentration in ECP groups were higher than those in ischemic groups(P<0.05).The NO levels and NOS specific activity in myocardium of ischemic dogs were lower than those in controls and ECP group(P<0.05).Protein synthesis of iNOS increased and that of eNOS decreased in ischemic myocardium.But ECP could control the protein synthesis of iNOS, and increase that of eNOS.Further studies showed that the expression of cNOS mRNA decreased in ischemic myocardial tissue, ECP might promote the expression of it and regulate NOS in the gene level.CONCLUSION:The results suggested that it was one of the most important mechanisms through raising the NO levels to protect ischemic myocardium in ECP.  相似文献   

13.
AIM: To study the effects of cholecystokinin octapeptide (CCK-8) on cerebral cortex injury during endotoxic shock (ES) and its mechanisms. METHODS: Rabbits were injected intravenously with lipopolysaccharide (LPS, 8 mg/kg) to establish ES model. Rabbits (n=32, 8 in each group) were randomly assigned to receive one of four treatments intravenously: normal saline (as control), LPS, CCK-8 pretreatment 30 min before LPS, proglumide (Pro, nonspecific antagonist of CCK receptors) pretreatment 30 min before LPS. The changes of mean arterial pressure (MAP) were measured. The morphologic changes in cerebral cortex were observed through light microscope (LM) and transmission electron microscope (TEM). The alterations of activities of nitric oxide synthase (NOS) and superoxide dismutase (SOD), contents of nitric oxide (NO) and malondialdehyde (MDA) in cerebral cortex were assayed. The expressions of protein of inducible NOS (iNOS) and neuronal NOS (nNOS) were detected by immunohistochemistry staining in cerebral cortex in 4 groups of Sprague-Dawley (SD) rats (n=12, 3 in each group) which were grouped as that of the rabbits. RESULTS: LPS administration resulted in lower MAP than that in control group (P<0.01). Hydropic degeneration of neurons and severe injuries to capillaries were observed in cerebral cortex of ES rabbits. LPS administration induced the expression of iNOS protein in the cytoplasm of neurocytes, and lead to stronger positive signals of nNOS than that in control group. NOS activity, NO2ˉ/NO3ˉ level and MDA content were higher (P<0.05, P<0.01 and P<0.01), while SOD activity was lower in cerebral cortex of ES rabbits than those in control group (P<0.01). CCK-8 pre-administration alleviated the changes induced by LPS, while Pro pre-administration aggravated those alterations. CONCLUSION: CCK-8 protects brain tissues against the injury induced by LPS, which may be associated with its effects of suppressing the overproduction of NO and free radicals.  相似文献   

14.
AIM: To observe the effect of mesenteric lymph reperfusion (MLR) on the brain morphology and neurotransmitter in rats with superior mesenteric artery occlusion (SMAO) shock, and to explore the mechanism of oxygen free radicals, nitric oxide (NO), polymorphonuclear neutrophils (PMN), membrane ATPase function and energy metabolism. METHODS: Twenty-four male Wistar rats were randomly divided into 4 groups: in sham group, the rats were given only anesthetization and operation; in MLR group, the rats were performed 1 h occlusion of mesenteric lymphatics (ML) followed by 2 h of reperfusion; in SMAO group, the rats were performed 1 h occlusion of superior mesenteric artery (SMA) followed by 2 h of reperfusion; in MLR+SMAO group, the rats were performed 1 h occlusion of SMA and ML followed by 2 h of reperfusion. After 2 h of reperfusion, the brain tissue was taken for preparing microscopic sections to observe the morphological change. At the same time, the brain tissue was homogenized for determining the choline acetyltransferase (ChAT), acetylcholine esterase (AChE), dopamine (DA), norepinephrine (NE), lactic acid (LA), malondialdehyde (MDA), superoxide dismutase (SOD), NO, nitric oxide synthase (NOS), myeloperoxidase (MPO), cell membrane ATPase and ATP. RESULTS: Morphological observation showed that the architecture of the brain was close to normal in sham and MLR groups. Necrosis, degeneration and occasional swelling were found in neuronal cells in SMAO group, and in MLR + SMAO group the injury of the neurons was more serious than that in SMAO group. The contents of MDA, NO and LA, the activities of AChE, NOS and MPO in brain homogenate in SMAO and MLR+SMAO groups were increased, the ChAT activity and DA, NE contents were reduced significantly than those in MLR and sham groups, respectively. The contents of MDA and NO, the activities of AChE, NOS and MPO in MLR+SMAO group were higher than those in SMAO group. The activities of Na+-K+-ATPase and SOD in brain homogenate in SMAO group were lower than those in sham and MLR groups, the Mg2+-ATPase activity and ATP content were lower than those in MLR group. The activities of SOD, Na+-K+-ATPase, Ca2+-ATPase, Mg2+-ATPase and Ca2+-Mg2+-ATPase in brain homogenate in MLR+SMAO group were lower than those in sham and MLR groups, and the DA, Ca2+-ATPase, Mg2+-ATPase, Ca2+-Mg2+-ATPase and ATP were also lower than those in SMAO group. CONCLUSION: MLR exacerbates the brain injury, reduces the DA level and increases the AChE activity in SMAO shock rats, indicating that MLR enhances the brain tissue free radical injury, NO synthesis and releases, PMN detention, and decreases the activity of cell membrane ATPase, also induces the energy metabolism dysfunction.  相似文献   

15.
AIM: To explore the mechanism underlying inducible nitric oxide (NO) caused injury of endothelial cells during inflammation. METHODS:The activity of iso-enzymes of NO synthase (NOS), NO level and iNOS expression were examined using NADPH method, Griess reaction and RT-PCR, respectively. Furthermore, the lactate dehydrogenase (LDH) release rate, malondialdehyde (MDA) content were also measured. RESULTS:Co-administration of cytokines (TNF-α 5×105 U/L, IL-1β 2×105 U/L, INF-γ 2×105 U/L) and LPS (10 mg/L) caused an obvious increase in NOS activity, NO levels (about two-fold) and a significant injury of the cells. At the same time, a significant increase in iNOS mRNA was also detected. Wheareas, treatment of the cells separately with cytokines or LPS for 24 h had no significant effect on NOS activity and NO level in cell lysates, however, it caused a significant increase in LDH release and MDA content. Also, the effect of cytokines and LPS on cell viability was concentration-and time-dependent. L-NMMA, a inhibitor of NOS, can suppress inducible NO production and protect cells against NO induced injury. CONCLUSION:Co-administration of cytokines (TNF-α, IL-1β and INF-γ) and LPS significant activated iNOS and NO production which, in turn, induced oxidative reaction in endothelial cells.  相似文献   

16.
AIM: To explore the role of endogenous hydrogen sulfide (H2S) in the mechanism of cholecystokinin octapeptide (CCK-8) to alleviate acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: Eighty-four Sprague-Dawley rats were randomly divided into seven groups: control, LPS (instilled intratracheally to reproduce the model of ALI), NaHS (H2S donor) +LPS, propargylglycine ［inhibitor of cysathionine-γ-lyase (CSE), PPG］+LPS, CCK-8+LPS, PPG+CCK-8+LPS and CCK-8 group. Animals were sacrificed at 4 h and 8 h after agent instillation. The wet and dry ratio (W/D) of the lung weight was measured and calculated. Morphological changes of lung tissues were observed. H2S concentration in plasma, malondialdehyde (MDA) content, myeloperoxidase (MPO) and CSE activities in the lung were determined. Furthermore, the level of P-selectin of lung tissue was measured by radioimmunoassay, the CSE mRNA expression in the lung was detected by RT-PCR, and the protein content in bronchoalveolar lavage fluid (BALF) was detected. RESULTS: Compared with control, severe injury of lung tissues and increase in W/D, protein content in BALF, MDA content, MPO activity and P-selectin level in the lung were observed in rats treated with LPS. LPS also lead to a drop in plasma H2S concentration, lung CSE activity and CSE mRNA expression. Administration of NaHS before LPS could attenuate the changes induced by LPS, while H2S concentration, CSE activity and CSE mRNA expression were higher than those in LPS group. However, pre-treatment with PPG exacerbated the lung injury induced by LPS, H2S concentration, CSE activity and CSE mRNA expression were lower than those in LPS and CCK-8 +LPS group, respectively. CONCLUSION: CCK-8 attenuates LPS-induced acute lung injury by means of anti-oxidation and inhibition of PMN adhesion and aggregation, both of which are mediated by endogenous H2S.  相似文献   

17.
  相似文献   

18.
AIM:To study the effect of Toll-like receptor 4 (TLR4) on the secretion of inflammatory factors in the pancreatic acinar AR42J cells induced by lipopolysaccharides (LPS). METHODS:The rat pancreatic acinar AR42J cells were treated with LPS. The expression of TLR4 at mRNA and protein levels was determined by real-time PCR and Western blot. The lentivirus carrying TLR4 small interfering RNA (siRNA) was used to infect the AR42J cells. Under LPS stimulation, the interference efficacy was measured by real-time PCR and Western blot. The cell viability was measured by MTT assay, and the leakage rate of lactate dehydrogenase (LDH) was examined by dinitrophenylhydrazine method. The releases of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the cell culture medium were detected by ELISA, and the malondialdehyed (MDA) content in supernatant was measured by thiobarbituric acid method. The activity of superoxide dismutase (SOD) in the supernatant was determined by xanthine oxidation, and the activity of glutathione peroxidase (GSH-Px) and catalase (CAT) was detected by colorimetry. RESULTS:The expression of TLR4 at mRNA and protein levels in LPS-treated AR42J cells was significantly increased (P<0.05). Infection with TLR4 siRNA-carrying lentivirus significantly inhibited the expression of TLR4 at mRNA and protein levels in the AR42J cells under LPS stimulation(P<0.05). The viability of AR42J cells was decreased after LPS treatment. The leakage rate of LDH was increased, the levels of IL-1β and TNF-α secreted by the AR42J cells were increased, the content of MDA was increased in the supernatant, and the activity of SOD, GSH-Px and CAT was reduced (P<0.05). After knock-down of TLR4 expression, the viability of AR42J cells was increased under LPS stimulation, the LDH leakage rate, secreted levels of IL-1β and TNF-α, and the content of MDA in cell culture medium were decreased, and the SOD, GSH-Px and CAT levels were increased (P<0.05). CONCLUSION:LPS induces the expression of TLR4 in the pancreatic acinar AR42J cells. Knock-down of TLR4 expression reduces the secretion of inflammatory factors IL-1β and TNF-α, and attenuates the oxidative damage in pancreatic acinar AR42J cells induced by LPS.  相似文献   

19.
AIM: To observe the effect of endogenous nitric oxide synthase(NOS) inhibitor asymmetric dimethylarginine(ADMA) and its signaling pathways on NO levels and skeletal muscle contractility in 4-week running rats. METHODS: The 4 weeks running rat model was established. The twitch tension, tetanic tension and the fatigue test of soleus muscle induced by electrical stimulation ex vivo were detected. The ATP content, mitochondrial DNA levels and the mRNA expression of peroxisome proliferator-activated receptor γ coactivator-1α(PGC-1α), nuclear respiratory factor(NRF) were measured to reflect the mitochondrial function and biosynthesis in the skeletal muscle. Serum ADMA concentration was detected by high performance liquid chromatography. The endogenous ADMA enzymes PRMT1 and 2 subtypes of ADMA metabolism enzyme DDAH, 3 subtypes of NOS protein expression in the skeletal muscle were determined by Western blot. NOS activity and nitric oxide(NO) content were analyzed by colorimetric method. RESULTS: Compared with normal control group, the twitch tension, tetanic tension and the anti-fatigue capability of soleus muscle in running group were significantly enhanced, ATP content, mitochondrial DNA content and the mRNA expression of PGC-1α and NRF were significantly increased(P<0.01). In addition, the protein expression of constitute type NOS(cNOS) and NOS activity were significantly increased(P<0.01), but the increase in NO content was relatively smaller in soleus muscle in exercise group(P<0.05). Moreover, serum ADMA concentration in running group was increased, while the DDAH2 expression in skeletal muscle was decreased.CONCLUSION: Short-term endurance exercise enhances the twitch tension, tetanic tension and fatigue resistance of soleus muscle. The mechanism may be that increased cNOS expression feedbacks to increase ADMA concentration, thus maintaining the increase in NO synthesis at a relatively low level, and resulting in promoting skeletal muscle mitochondria biosynthesis and mitochondrial function.  相似文献   

20.
  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号