Specific heat of single-crystal PrMnO3.

The specific heat of single-crystal PrMnO3 was investigated from 2 to 200 K under different magnetic fields up to 8 T. A Schottky-like anomaly observed at low temperature was gradually shifted to higher temperatures by magnetic fields. The first four singlets of the Pr3+ 3H4 ground multiplet in PrMnO3 are given for the first time by fitting the specific heat of Pr3+ ions below 40 K under zero field. By analysing the field dependence of the first singlet of Pr3+ ions, the Pr-Mn exchange field is found to be negligible, which is consistent with the magnetic anisotropy of Pr3+ ions revealed in the magnetic measurement. At TN, the cooperative antiferromagnetic ordering of Mn3+ spins shows up as λ-shaped anomaly, which is lowered and broadened in magnetic fields. The magnetic entropy near TN is estimated by subtracting the contributions to specific heat from Pr3+ ions and lattice vibrations. It was found that the fraction of entropy above TN in the total entropy increases with the fields due to the enhancement of spin fluctuations by magnetic field.

Effects of Coriolus versicolor polysaccharides peptides on electric activity of mediobasal hypothalamus and on immune function in rats.

AIM: The nervous mechanism of the immune potentiating effect of Coriolus versicolor polysaccharides peptides (PSP) was studied in Wistar rats. METHODS: The unit discharge of the mediobasal hypothalamus (MBH) neurons was recorded extracellularly and the lymphocyte proliferation was measured. RESULTS: PSP 1 g.kg-1 ig for 5 d increased the T-lymphocytes and promoted T-lymphocyte proliferation in spleen and peripheral blood. This promoting effect of PSP was blocked by MBH lesion. PSP increased the discharge frequency of MBH neurons, but no increase in discharge frequency was observed after treatment of PSP plus immune inhibitor, cyclosporin A. CONCLUSION: MBH is involved in the immune-potentiating effect of PSP.

Effects of Panax notoginseng saponins on posthypoxic cell damage of neurons in vitro.

AIM: To study cerebral protective mechanism of Panax notoginseng saponins (PNS). METHODS: Cultured neurons of chick embryo cerebral hemisphere were used as an in vitro system for investigating the effects of PNS. The hypoxic cell damage of neurons cultured were induced by NaCN. The levels of adenosine triphosphate (ATP) were determined with HPLC. PNS was added 30 min before, beginning or after hypoxia. RESULTS: PNS 50 and 100 mg L-1 retarded the break down of ATP of cultured neurons after 2-h hypoxia for 11.3 +/- 1.5 (P < 0.05) and 12.8 +/- 2.2 mumol/g protein (P < 0.01), respectively and accelerated the restoration of ATP during 30-min reoxygenation for 21.0 +/- 2.0 (P < 0.05) and 22.7 +/- 2.6 mumol/g protein (P < 0.01), respectively. PNS also reduced the release of creatine kinase (CK) from 75 +/- 8 kU L-1/g protein to 52 +/- 6 (P < 0.05) and 41 +/- 3 kU L-1/mg protein (P < 0.01), respectively and promoted the restoration of ATP of neurons 20 h after hypoxia when administered in the beginning of hypoxia from 13.0 +/- 0.9 mumol/g protein to 18.1 +/- 1.4 and 20.5 +/- 2.1 mumol/g protein (P < 0.01), respectively. PNS still promoted the restoration of ATP from 13.0 +/- 0.9 nmol/mg protein to 14.9 +/- 1.0 and 18.3 +/- 0.7 nmol/mg protein (P < 0.01), respectively and reduced (PNS 100 mg L-1) the CK release of neurons 20 h after hypoxia even when added in the recovery. CONCLUSION: The protection against hypoxic damage of PNS was related to improving energy metabolism, preserving the structural integrity of neurons.

Effects of quercetin on Na(+)-K(+)-exchanging ATPase and Ca(2+) Mg(2+)-ATPase in rats.

Quercetin (Que) ig 200 mg.kg-1, qd x 14 d decreased activities of the Na(+)-K(+)-exchanging ATPase (I) of rat brain plasma membranes and heart sarcolemmal and Ca(2+) Mg(2+)-ATPase (II) of heart sarcolemmal membrane. Que 100 mg.kg-1 reduced the activity of I from rat heart sarcolemmal preparation, but had no effect on that from rat brain plasma membranes. The result shows that I of myocardium is more sensitive than that of brain in rat. Que also showed a remarkable inhibitory effect in the II of heart sarcolemma.

Effects of quercetin on platelet and reperfusion-induced arrhythmias in rats.

The role of platelets in reperfusion arrhythmias (RA) and the efficacy of quercetin (Que) in preventing the arrhythmias were investigated in anesthetized rats. Platelet count (PC) was performed, the ultrastructure of platelets was scrutinized, and the levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (Keto-PGF1 alpha) in plasma were determined by radioimmunoassay (RIA). The pretreatment with Que (5 mg.kg-1) 2 min prior to reperfusion inhibited RA. Que remarkably improved the ultrastructural deviation of platelet, inhibited the platelet aggregation and thromboxane A2 (TXA2) formation, and increased the prostacyclin (PGI2) generation and the ratio of PGI2/TXA2. The decrease in PC and increase in TXB2 level in plasma indicated the participation of platelets in the arrhythmogenic activity of ischemia and reperfusion. The results showed that Que produced a protective effect against RA probably through inhibiting the platelet aggregation, TXA2 formation and increasing the PGI2 generation.

[Effect of quercetin on chemiluminescence of human platelets induced by arachidonic acid].

Arachidonic acid (AA)-induced platelet chemiluminescence (CL) was measured with a lumiphotometer. Quercetin remarkably inhibited the CL, the IC50 of quercetin was 3 mumol.L-1. When quercetin plus aspirin, which inhibits only cyclooxygenase, was added, the inhibitory rate of platelet-CL obviously increased (P < 0.01). On the other hand, the quercetin had a scavenging effect on superoxide anion radical using alkaline sodium dithionite solution generation. The IC50 was 20.9 mumol.L-1. In addition, superoxide dismutase of 0.1 mg.ml-1 inhibited the platelet-CL by 97.8%, while mannitol, a hydroxyl radical scavenger, only by 43.3% at a concentration of 80 mg.ml-1. These results suggest that the mechanism of the inhibiting AA-induced platelet-CL by quercetin was associated with scavenging the superoxide anion radical directly and with inhibiting the cyclooxygenase.

[Effects of piracetam on Na(+)-K(+)-ATPase and monoamine oxidase in rat brain and its antioxidation effect].

Piracetam, ig 600 mg.kg-1.d-1 for 30 d, caused a 20% decrease in the activity of Na(+)-K(+)-ATPase and monoamine oxidase (MAO) in vivo. In vitro, it presented an inhibitory effect on MAO, but had no direct effect on Na(+)-K(+)-ATPase at a concentration of 100 mmol.L-1. Piracetam had a potential action in scavenging free radicals. This action may be related to its clinical effects on amnesia and Alzheimer's disease.