Opposing needling promotes behavior recovery and exerts neuroprotection via the cAMP/PKA/CREB signal transduction pathway in transient MCAO rats.

The aim of the present study was to investigate whether the cyclic adenosine 3',5'­monophosphate (cAMP)/protein kinase A(PKA)/cAMP­responsive element binding protein (CREB) signal transduction pathway triggered by γ­aminobutyric acid class B (GABA(B)) receptor activation is involved in neuroprotection against ischemia and behavioral recovery induced by opposing needling (ON). A total of 80 rats were randomly divided into four groups: A sham operation group, an ischemia group, an ON group and an ON group effectively inhibited by the GABA(B) receptor antagonist, CGP35384 (n=20/group). The behavior of the rats was assessed by their neurological deficit score, whereas the impairment of gait was examined using the CatWalk system. The volume of cerebral infarction was examined upon treatment with 2,3,5­triphenyltetrazolium chloride. The expression levels of CREB, GABA(B1) and GABA(B2) were examined by western blotting and reverse transcription­quantitative polymerase chain reaction, and the activity of adenylyl cyclase (AC), cAMP and PKA in the serum was detected using an enzyme­linked immunosorbent assay. In the present study, in comparison with other groups, the ON group exhibited a reduced score for the neurological deficit, the stride length and swing speed were improved, and the volume of infarction was reduced. However, these effects were reversed upon administration of CGP35384. Additionally, the expression levels of CREB, GABA(B1) and GABA(B2) were increased in the ON group. The levels of AC, cAMP and PKA in the serum were also increased in the ON group, whereas the addition of CGP35384 reversed these effects. The results of the present study demonstrated that ON markedly protected the brain against transient cerebral ischemic injury, and this effect was possibly mediated by the activation of the GABAB/cAMP/PKA/CREB signal transduction pathway. These findings implied that ON may be a potential therapeutic method for treating stroke.

[Effects of supplemented taohe chengqi decoction in treating insulin resistance in rats with non-insulin dependent diabetes mellitus].

OBJECTIVE: To investigate the effect of Supplemented Taohe Chengqi Decoction (STHCQD) in treating non-insulin dependent diabetes mellitus (NIDDM). METHODS: The model of rats with NIDDM was formed with injection of streptozotocin and fed on high calorie diet to study the effects of STHCQD on the release of insulin mediator from liver cell membranes, the glucose oxidation in adipocytes as well as the insulin sensitivity. RESULTS: (1) Fasting serum glucose, serum insulin, intake of food and water were significantly decreased (P < 0.05-0.01) in STHCQD-treated diabetic rats as compared with untreated diabetic rats, while the insulin sensitivity was significantly increased (P < 0.05). (2) The liver cell membranes from STHCQD-treated diabetic rats released the quantity of insulin receptor which inhibited adenylate cyclase activity, but this effect was blunted in untreated diabetic rats (P < 0.05). (3) A significantly increased glucose oxidation in adipocyte of STHCQD-treated diabetic rats was found as compared with those of untreated diabetic rats (P < 0.05). CONCLUSIONS: STHCQD therapy increased sensitivity and responsiveness of target cells to insulin, i.e., it might decrease insulin resistance at receptor sites and postreceptor sites in rats with NIDDM, but could not reverse the insulin resistance.

[The effect of intensified lipid peroxidation in patients with Devergie's lichen ruber pilaris on adenylate cyclase activity]. / Vliianie usilennoi peroksidatsii lipidov u bol'nykh krasnym volosianym lishaem Deverzhi na aktivnost' adenilattsiklazy.

Studies with the use of Fe2(+)-induced chemiluminescence of apo-beta-lipoproteins and electron histochemistry have revealed that PUVA therapy and vitamin A high doses enhance lipid peroxidation and activate adenylate cyclase in patients with Devergie's disease. This finding permits a conclusion on the usefulness of enhancing lipid peroxidation in order to reduce cellular mitotic activity.

Isolation of inhibitors of adenylate cyclase from dan-shen, the root of Salvia miltiorrhiza.

The effect of dan-shen extract, the root of Salvia miltiorrhiza, on adenylate cyclase was investigated in both rat brain and rat erythrocytes. The EtOAc fraction of the MeOH extract was proved to have significant inhibitory activity. Potent inhibitory principles in the EtOAc fraction were isolated and identified as 4 polyphenolic acids, rosemarinic acid, lithospermic acid, and their methyl ester derivatives.

Human monocyte killing of Staphylococcus aureus: modulation by agonists of cyclic adenosine 3',5'-monophosphate and cyclic guanosine 3',5'-monophosphate.

This study was designed to test whether cyclic nucleotides play a role in the regulation of bacterial killing by human monocytes. Agents were tested for their ability to activate monocyte adenylate or guanylate cyclase in cell-free preparations, to increase cyclic adenosine 3',5'-monophosphate (cAMP) or cyclic guanosine 3',5'-monophosphate (cGMP) in intact human monocytes, and to modulate monocyte-induced killing of Staphylococcus aureus in vitro. Prostaglandin E1 and cholera toxin activated monocyte adenylate cyclase and inhibited monocyte killing of S. aureus. An adenylate cyclase inhibitor, RMI 12330A, reversed the prostaglandin E1-mediated inhibition of bacterial killing, thus implicating cAMP as the intracellular mediator of this inhibition. In contrast, monocyte cGMP levels were increased 5- and 17-fold by 5-hydroxytryptamine and N-methyl-N' -nitro-N-nitrosoguanidine, respectively, but neither agent was effective in modulating monocyte bactericidal activity. Thus, modulation of bactericidal activity in human monocytes did not conform to the yin/yang theory of opposing actions by cAMP and cGMP, for although monocyte-mediated killing of S. aureus was inhibited by cAMP agonists, it was not enhanced by cGMP agonists.