Protective effects of P2X7 receptor inhibition in cerebral ischemia/reperfusion injury in rats / 中南大学学报(医学版)

To investigate the protective effects of P2X7 receptor (P2X7R) inhibitor against cerebral ischemia/reperfusion (I/R) injury in rats and the possible mechanisms.
 Methods: The neurological deficit of rats was evaluated by Longa score. The infarct volume was examined by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining. The expression levels of extracellular signal-regulated kinase (ERK), phosphorylation extracellular signal-regulated kinas p-ERK), connexin 43 (Cx43), Bax, Bcl-2 and cleaved caspase-3 were detected by Western blot.
 Results: Compared with sham group, the neurobehavioral score (P<0.05) and cerebral infarct volume (P<0.01) of rats in I/R group was increased. Compared with I/R group, brilliant blue G (BBG, the antagonist of P2X7R) or PD98059 (the inhibitor of EKR kinase) could reduce the neurobehavioral score (P<0.01) and cerebral infarct volume significantly (P<0.05). The neurobehavioral score and cerebral infarct volume was further decreased (P<0.05) when rats were treated with both BBG and PD98059. Compared with I/R group, the expression levels of p-ERK, Cx43, cleaved caspase-3 and the ratio of Bax/Bcl-2 were decreased by BBG or PD98059 pretreatment, and the protective effects were further enhanced when rats were treated with both BBG and PD98059 (P<0.05).
 Conclusion: Inhibition of P2X7R reduces the cerebral I/R injury of rats. ERK inhibition is probably involved in the protective effects of P2X7R inhibitor against cerebral I/R injury, which may be related to the reduction of Cx43 and cleaved caspase-3, and the ratio of Bax/Bcl-2.

Protective effect of propofol against cerebral ischemic/reperfusion injury may involve inhibition of gap junction / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the protective effect of propofol against focal cerebral ischemia/reperfusion (I/R) injury in rats and its relation with gap junction.</p><p><b>METHODS</b>Seventy adult male SD rats were randomly divided into sham-operated group, I/R group, low-, moderate-, and high-dose propofol groups (25, 50, 100 mg/kg; P25, P50, P100 groups, respectively), I/R+CBX group and P100+CBX group. Thread occlusion was used to induce middle cerebral artery occlusion (MCAO) in the mice for 2 h followed by reperfusion for 24 h. Longa's scores were used to evaluate the neurological behavior of the rats. TTC staining was used to measure the cerebral infarction volume and Western blotting was performed to detect the expressions of Cx43, PKC, Bax, and Bcl-2 in the brain of the rats.</p><p><b>RESULTS</b>Compared with the I/R group, the rats pretreated with moderate and high doses of propofol showed significantly reduced neurological behavior scores and cerebral infarction volume percentage, and the effect was more obvious in high-dose propofol pretreatment group. CBX obviously enhanced the protective effect of propofol against I/R injury. Compared with those in the sham-operated group, the protein expression of Cx43 and the Bax/Bcl-2 ratio were increased and the protein expression of PKC was reduced in I/R group, and these changes were significantly reversed by high-dose propofol pretreatment; the effects of propofol were further enhanced by CBX.</p><p><b>CONCLUSION</b>The protective effect of propofol against cerebral I/R injury may involve the inhibition of the gap junction via PKC signaling and by reducing the Bax/Bcl-2 ratio.</p>

Protective effect of NADPH oxidase against cerebral ischemia/reperfusion injury / 中国药理学通报

Aim To determine the protective effect of NADPH oxidase against focal cerebral ischemia/reper-fusion ( I/R) injury in rats. Method A thread occlu-sion method was used to make a middle cerebral artery occlusion ( MCAO ) model. Apocynin ( 2. 5 mg · kg-1 ) was injected by tail vein 15 min before ischemi-a. Then, the neurological behavior, cerebral infarction volume, pathological morphological changes and the expression of Cx36, PKC, Bax, Bcl-2 of rats were de-tected after ischemia for 2 h, followed by reperfusion for 24 h. Results Compared with cerebral I/R group, administration of apocynin significantly reduced the neurological behavior scores and the cerebral in-farction volume percentage, alleviated the pathological morphological damage, increased the protein expres-sion of Cx36 and PKC, and reduced the Bax/Bcl-2 ra-tio of rats with focal cerebral I/R injury. Compared with apocynin group , apocynin combined with PKC inhibitor significantly reduced above protective effects. Conclusion Inhibition of NADPH oxidase could alle-viate cerebral I/R injury, increase the levels of Cx36, PKC proteins and reduce the Bax/Bcl-2 ratio.

Tc1/Tc2 Imbalance in the Peripheral Blood of Patients with Recurrent Genital Herpes / 华中科技大学学报（医学）（英德文版）

In order to investigate the IFN-γ and IL-4 expression of CD8+ T lymphocytes in the peripheral blood from patients with recurrent genital herpes (RGH) at different clinical periods and their relationship with the pathogenesis of RGH, flow cytometry was used to detect the intracellular cytokines (IFN-γ and IL-4) of CD8+ T lymphocytes in the peripheral blood of 30 patients with RGH at acute period, 20 patients with RGH at recovery period and 15 healthy volunteers. The results showed that RGH patients at acute period had a lower percentage of Tc1 subsets in peripheral blood than that of healthy controls (P＜0. 001), especially a remarkable decreased percentage of Tc1 subsets (P＜0. 001) among those RGHpatients with recurrent number more than 3 in the recent half a year. Tc1/Tc2 ratio in the RGH patients at acute period was significantly decreased as compared with normal control group (P＜0.05). The recurrent number of acute patients in the recent half a year was significantly correlated with the percentage of Tc1 subsets and the ratio of Tc1/Tc2 (P＜0.05). A decreased percentage of Tc1 subsets was found among the RGH patients with recurrent number more than 3 in the recent half a year at recovery period in comparison with healthy volunteers (P＜0.05), and it was significantly correlated with the recurrent number in the recent half a year (P＜0.05). It is concluded that there are Tc1/Tc2 imbalance and a low level of Tc1 subsets in RGH patients who are relapsing repeatedly in the near period. The low level of Tc1 subsets maybe an important factor for the recurrence of RGH and the reactivation of latent herpesvirus infection.

Regulations of Human Tumor Necrosis Factor and Recombinant Human Interferon-? on activity of Human Polymorphonuclear Neutrophils against Candida albicans / 中华皮肤科杂志

This paper studies tile regulation of cytokines such as human tumor necrosis(Hu-TNF) and recombinant human interferon - (rHu -IFN - ) on activity of human polymorphonuclear neutrophils (PMN) against Candida albicans by determing numbers of colony - forming unit of Candida albicans. We detected that Hu - TNF and rHu IFN st did not interfere directly with fungal growth. These two cytokines enhanced PMN to inhibit Candida albicans growth. When preincubating PMN with Hu --TNF and rHu-IFN -togather, the activity of PMN against Candidaalbicans was synergically enhanced. The degree of enhancement of the activity of PMN againstCandida albicans was highly dependent on these two cytokines - PMN preincubation time. Thus,Hu -- TNF and rHu -- IFN -- have the ability to activate PMN, and the synergistic action of thetwo cytokines may prove clinically effective for increasing the ability of immuncompromised hosts against opportunistic fungal infectons.