OBJECTIVETo investigate the polymorphism of FcgammaRIIIb genotype, IgG G2m(23) factor and their associations with the susceptibility to aggressive periodontitis.

METHODSDNA of white blood cells and serum from 21 aggressive periodontitis patients and 26 healthy controls was extracted. Genotype of FcgammaRIIIb and phenotype of G2m(23) factor was determined by allele-specific PCR and dot immunobinding assay respectively.

RESULTSThe frequency of FcgammaRIIIb-NA1/NA1 genotype in aggressive periodontitis patients was significantly higher than in healthy controls (P < 0.05). The ratio of subjects with FcgammaRIIIb-NA1/NA1 genotype and positive G2m(23) factor was higher in aggressive periodontitis patients (11/21) than in health controls (5/26) (P < 0.05). However, no statistical difference in distribution of G2m(23) factor alone was observed between patients and controls.

CONCLUSIONSThis study indicates that FcgammaRIIIb-NA1/NA1 genotype may be a susceptible genotype to aggressive periodontitis in Chinese population. Subjects with FcgammaRIIIb NA1/NA1 genotype and positive G2m(23) factor may be more susceptible to aggressive periodontitis.

Adult ; Antigens, CD ; genetics ; Asian Continental Ancestry Group ; genetics ; Female ; GPI-Linked Proteins ; Genetic Predisposition to Disease ; Genotype ; Humans ; Immunoglobulin Gm Allotypes ; genetics ; Male ; Periodontitis ; genetics ; Receptors, IgG ; genetics

OBJECTIVETo study the effect of cerebral mild hypothermia on cerebral mitochondrial ATPase activities in neonatal rats with hypoxic-ischemic brain damage (HIBD).

METHODSEighty-four seven-day-old Wistar rats were randomly assigned into four groups: sham-operated normothermic, sham-operated mild hypothermic, HIBD normothermic and HIBD mild hypothemic. HIBD was induced by left common carotid artery ligation, followed by 8% hypoxia exposure. At each time interval of 2, 6, and 12 hrs post-hypoxia-ischemia (HI), 7 rats were sacrificed and the brain tissues were sampled for detecting the activities of mitochondrial Na+K+ATPase and Ca2+ATPase.

RESULTSThe activities of mitochondrial Ca2+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 2, 6, and 12 hrs post-HI. The HIBD mild hypothemic group had higher mitochondrial Ca2+ATPase activities compared with the HIBD normothermic group at 2, 6, and 12 hrs post-HI (5.25 +/- 0.61 micromol/mgPr.h vs 3.17 +/- 0.81 micromol/mgPr.h 4.59 +/- 0.81 micromol/mgPr.h vs 2.26 +/- 0.53 micromol/mgPr.h4.61 +/- 0.62 micromol/mgPr.h vs 1.31 +/- 0.78 micromol/mgPr.H, respectively) (P < 0.01). The activities of mitochondrial Na+K+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 6 and 12 hrs post-HI. A significant difference was observed in the mitochondrial Na+K+ATPase activities between the HIBD mild hypothemic and HIBD normothermic groups at 6 and 12 hrs post-HI (5.25 +/- 0.66 micromol/mg Pr.h vs 3.76 +/- 0.78 micromol/mgPr.h, 4.74 +/- 0.80 micromol/mgPr.h vs 3.12 +/- 0.53 micromol/mgPr.h; P < 0.01).

CONCLUSIONSMild hypothermia following HIBD inhibits the decline in cerebral mitochondrial Ca2+ and Na+K+ ATPase activities in neonatal rats, thus providing protective effects against HIBD.

Animals ; Animals, Newborn ; Brain ; enzymology ; Calcium-Transporting ATPases ; metabolism ; Female ; Hypothermia, Induced ; Hypoxia-Ischemia, Brain ; enzymology ; therapy ; Male ; Mitochondria ; enzymology ; Rats ; Rats, Wistar ; Sodium-Potassium-Exchanging ATPase ; metabolism

Adult ; Calcium-Transporting ATPases ; metabolism ; Erythrocyte Membrane ; metabolism ; Female ; Humans ; Hydrocarbons ; adverse effects ; Lipid Peroxidation ; Male ; Middle Aged ; Occupational Exposure ; Sodium-Potassium-Exchanging ATPase ; metabolism ; Young Adult

The purpose of the present study was to investigate whether interleukin-2 (IL-2) changes the activity of sarcoplasmic reticulum (SR) Ca(2+) ATPase, sarcolemmal Ca(2+)ATPase and Na(+)/K(+) ATPase by measuring the Pi liberated from ATP hydrolysis with colorimetrical methods. It was shown that the activity of Ca(2+)ATPase in SR from IL-2-perfused (10, 40, 200, 800 U/ml) rat heart increased dose-dependently. After incubation of the SR with ATP (0.1 approximately 4 mmol/L), the activity of SR Ca(2+)ATPase increased dose-dependently in the control group. In the SR from 200 U/ml IL-2-perfused hearts, the activity of Ca(2+)ATPase was much higher than that in the control group. On the other hand, incubation of the SR with Ca(2+) (1 approximately 40 micromol/L) increased the activity of SR Ca(2+) ATPase in the control group. The activity of SR Ca(2+)ATPase of IL-2-perfused hearts was inhibited as the function to Ca(2+). Pretreatment with specific kappa-opioid receptor antagonist nor-BNI (10 nmol/L) for 5 min attenuated the effect of IL-2 (200 U/ml) on the activity of SR Ca(2+) ATPase. After pretreatment with pertussis toxin (PTX, 5 mg/L) or U73122 (5 micromol/L), IL-2 failed to increase SR Ca(2+)ATPase activity. The activity of SR Ca(2+)ATPase was not changed by incubation of SR isolated from normal hearts with IL-2. Perfusion of rat heart with IL-2 did not affect the activity of sarcolemmal Ca(2+)ATPase and Na(+)/K(+)ATPase. It is concluded that perfusion of rat heart with IL-2 increases the activity of SR Ca(2+)ATPase dose-dependently, which is mainly mediated by cardiac kappa-opioid receptor pathway including a PTX sensitive Gi-protein and phospholipase C. IL-2 increases the activity of SR Ca(2+)ATPase as the function to ATP, but inhibits the activity of SR Ca(2+)ATPase as the function to Ca(2+). IL-2 has no effect on the activity of sarcolemmal Ca(2+)ATPase and Na(+)/K(+)ATPase.
Animals ; Interleukin-2 ; pharmacology ; Male ; Myocardium ; enzymology ; Rats ; Rats, Sprague-Dawley ; Sarcolemma ; enzymology ; Sarcoplasmic Reticulum ; enzymology ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; metabolism ; Sodium-Potassium-Exchanging ATPase ; metabolism

Animals ; Brain ; drug effects ; metabolism ; Calcium-Transporting ATPases ; metabolism ; Female ; Mice ; Mice, Inbred Strains ; Polychlorinated Dibenzodioxins ; toxicity ; Sodium-Potassium-Exchanging ATPase ; metabolism

This study aimed to observe the general state and changes in pathophysiological indexes of multiple cerebral infarction rat model with Qi-deficienty and Blood-stasis syndrome. Rats were randomly divided into 4 groups(with 30 in each group): the normal group, the sham group, the model group and the Yiqi Huoxue recipe group. Rats in the model group and Yiqi Huoxue group were provided with interruptable sleep deprivation for 7 days before the multiple cerebral infarction operation, and followed by another 4 weeks of sleep deprivation; rats in the Yiqi Huoxue group were intragastrically administrated with drug at a dose of 26 g·kg⁻¹, once a day for 4 weeks. The general state was observed, and the pathophysiological indexes were measured at 48 h, 2 weeks and 4 weeks after administration. The results showed that rats in the normal group and the sham group represented a good general state and behaviors, with a normal morphological structure of brain tissues; rats in the model group featured yellow fur, depression, accidie, loose stools and movement disorder, with obvious brain histomorphological damage, which became aggravated with the increase of modeling time; rats in the Yiqi Huoxue group showed release in the general state and above indexes. Compared with the sham group at three time points, rats in the model group showed decrease in body weight, exhaustive swimming time and RGB value of tongue surface image, and increase in whole blood viscosity of the shear rate under 5, 60 and 150 S⁻¹, reduction in cerebral cortex Na⁺-K⁺-ATPase, Ca²⁺-ATPase activity and contents of 5-HT, rise in TXB2 levels and decline in 6-keto-PGF1a in serum(<0.05, <0.01). Compared with the model group, rats in the Yiqi Huoxue group showed alleviations in the above indexes at 2 w and 4 w(<0.05, <0.01). The results showed that the characterization and pathophysiological indexes in the multiple cerebral infarction rat model with Qi-deficiency and blood-stasis syndrome were deteriorated; Yiqi Huoxue recipe could significantly alliviate the abnormal conditions, which suggested of the model was stable and reliable and the pathophysiologic evolutionary mechanism might be related to energy metabolism dysfunction, vasoactive substance abnormality and changes in neurotransmitters.
Animals ; Calcium-Transporting ATPases ; metabolism ; Cerebral Infarction ; physiopathology ; Drugs, Chinese Herbal ; pharmacology ; Energy Metabolism ; Medicine, Chinese Traditional ; Qi ; Rats ; Sodium-Potassium-Exchanging ATPase ; metabolism

The aim of this research is to investigate the effects of paeoniflorin and menthol on the physiological function of Calu-3 cell membrane during the transport of puerarin. Calu-3 cell was used as the cell model to simulate nasal mucosa tissues, and the cell membrane fluidity, Na⁺-K⁺-ATPase activity and Ca²⁺-ATPase activity were detected by fluorescence recovery after photobleaching(FRAP) and ultramicro enzyme activity testing, in order to explore the mechanism of compatible drugs on promoting puerarin transport. The results showed that when puerarin associated with low, middle and high concentration of menthol or both paeoniflorin and menthol, the fluorescence recovery rate was increased significantly, while Na⁺-K⁺-ATPase activity had no significant change and Ca²⁺-ATPase activity was enhanced significantly as compared with puerarin alone. Therefore, it was concluded that menthol had the abilit of promoting the transport and the mechanism might be related to increasing membrane fluidity and activating Ca²⁺-ATPase.
Calcium-Transporting ATPases ; metabolism ; Cell Line, Tumor ; Cell Membrane ; Glucosides ; chemistry ; Humans ; Isoflavones ; metabolism ; Membrane Fluidity ; Menthol ; chemistry ; Monoterpenes ; chemistry ; Sodium-Potassium-Exchanging ATPase ; metabolism

OBJECTIVETo investigate the mechanism of the negative inotropic effect of tumor necrosis factor-alpha (TNF-alpha) in cardiomyocytes.

METHODSThe spectrofluorometric method was used to verify the calcium handling of the single myocyte. The activities of Ca(2+)-ATPase of sarcoplasmic reticulum (SR) and the activities of Ca(2+)-ATPase and Na(+)/K(+)-ATPase of plasma membrane were measured with colorimetric methods.

RESULTSTNF-alpha at 20 U/ml and 200 U/ml depressed the contractility of ventricular papillary muscle to 91% and 76% of control (P<0.01) respectively, but had no effect on the amplitude of electrically induced calcium transient in single myocyte. TNF-alpha inhibited the responsiveness of SR Ca(2+)ATPase activity to ATP (0.1 - 4 mmol/L) and Ca(2+) (1 - 40 micromol/L). TNF-alpha did not alter the activities of Ca(2+)-ATPase and Na(+)/K(+)-ATPase of plasma membrane compared with control group.

CONCLUSIONTNF-alpha decreases the myocardial contractility, at least partly, by inhibiting the activity of SR Ca(2+)- ATPase.

Animals ; Calcium ; metabolism ; Calcium-Transporting ATPases ; metabolism ; Depression, Chemical ; In Vitro Techniques ; Male ; Myocardial Contraction ; drug effects ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium-Potassium-Exchanging ATPase ; metabolism ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo assess any direct effect of extract of Paris polyphylla Simth (EPPS), a Chinese plant, on a cardiomyocyte subject to ischemia-reperfusion injury and to further elucidate its protective effect against myocardium ischemia on the cellular level.

METHODSNeonatal rat cardiomyocytes were isolated and subjected to an anoxia-reoxia injury simulating the ischemia-reperfusion injury in vivo in the presence or absence of EPPS or diltizem, a positive control. The lactate dehydrogenase (LDH) activities in culture supernatants and cell viabilities were analyzed using the enzymatic reaction kinetics monitoring-method and MTT method, respectively. Free intracellular calcium concentrations and activities of Na(+)-K(+) ATPase and Ca(2+) ATPase in cells were also measured with laser confocal microscopy and the inorganic phosphorus-transformation method, respectively.

RESULTSIn cardiomyocytes subject to anoxia-reoxia injury, EPPS at 50-400 mg/L showed a concentration-dependent inhibition on LDH leakage and maintenance of cell viability, and the effect was significant at 275 and 400 mg/L (both P<0.01). In addition, EPPS at 275 and 400 mg/L significantly inhibited the increase in intracellular free calcium (both P<0.01) as well as decreased the activities of Na(+)-K(+) ATPase and Ca(2+) ATPase (P<0.01, P<0.05).

CONCLUSIONSEPPS prevents anoxia-reoxia injury in neonatal rat cardiomyocytes in vitro by preservation of Na(+)-K(+) ATPase and Ca(2+) ATPase activities and inhibition of calcium overload. The direct protective effect on cardiomyocytes may be one of the key mechanisms that underlie the potential therapeutic benefit of EPPS against myocardium ischemia.

Animals ; Calcium ; metabolism ; Calcium-Transporting ATPases ; metabolism ; Cells, Cultured ; Hypoxia ; metabolism ; prevention & control ; Liliaceae ; chemistry ; Microscopy, Fluorescence ; Myocardium ; enzymology ; Plant Extracts ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; prevention & control ; Sodium-Potassium-Exchanging ATPase ; metabolism

OBJECTIVETo study characteristics of energy metabolism in the skeletal muscle of rats with postoperative fatigue syndrome (POFS) and the interventional effect of ginsenoside Rb1.

METHODWe chose resection of 70% of the "middle" small intestine as the rat model for POFS. Ninety-six adult male SPF SD rats were randomly divided into the control group, the model group, and the ginsenoside Rb1-treated group by body weight. And then, each group was further randomly divided into four subgroups, according to different postoperative investigated time points, such as postoperative day 1, postoperative day 3, postoperative day 7 and postoperative day 10. So the animals were divided into twelve subgroups (n = 8 in each subgroup). Rats of the control group and the model group were injected intraperitoneally with saline at the dose of 10 mL x kg(-1) one hour before the operation and once a day during the postoperative days. Rats of the ginsenoside Rb1-treated group were administered 10 mg x kg(-1) ginsenoside Rb1 by the same method. The skeletal muscles were sampled on postoperative day 1, 3, 7 and 10. The contents of ATP, ADP, AMP in skeletal muscles were determined by HPLC, and the activities of Na(+)-K(+)-ATPase and Ca(2+)-ATPase were investigated by colorimetry.

RESULTCompared with the control group, the content of ATP in skeletal muscle of rats of the model group decreased significantly on postoperative day 3 (P < 0.05), while the content of ADP significantly increased on postoperative day 7 and 10 (P < 0.05). The activity of Na(+)-K(+)-AT-Pase decreased on postoperative day 3 and 7 (P < 0.05), and the activity of Ca(2+)-ATPase decreased on postoperative day 7. After supplement of ginsenoside Rb1, on the investigated time points, all the negative changes of the indicators discovered above were significantly adjusted (P < 0.05) in rats of the ginsenoside Rb1-treated group, while no significant differences were investigated.

CONCLUSIONDuring a certain period of postoperative time, the activity of energy metabolism is depressed in the skeletal muscle of rats with POFS, but it can be improved by supplement of ginsenoside Rb1.

Animals ; Calcium-Transporting ATPases ; physiology ; Energy Metabolism ; drug effects ; Fatigue ; drug therapy ; metabolism ; Ginsenosides ; pharmacology ; therapeutic use ; Male ; Muscle, Skeletal ; metabolism ; Postoperative Complications ; drug therapy ; metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium-Potassium-Exchanging ATPase ; physiology ; Syndrome