[Study on safflower yellow for injection based on cell degranulation and acute anaphylactoid model].

This paper was aimed to establish screening methods of anaphylactoid reaction caused by safflower yellow for injection based on RBL-2 H3 cell degranulation model and mice model for acute anaphylactoid reaction,and evaluate the hypersensitivity caused by safflower yellow for injection from different batches. An in vitro cell model was used to keep the cells stimulated for an hour with different batches of safflower yellow for injection as the drug group,serum-free MEM medium as negative control group and 30 mg·L-1 C48/80 as positive control group respectively. The supernatant was then absorbed,and neutral red staining technique was used to detect the effect of safflower yellow injection on the degranulation of RBL-2 H3 cells with the positive cell rate of degranulation as the indicator.An in vivo model was established to validate the experimental results,and mice model for acute anaphylactoid reaction and ELISA method were adopted to detect the plasma histamine content,and screen the hypersensitivity caused by safflower yellow for injection at the animal level by using plasma histamine content as a test index. The results of the neutral red staining experiments showed that the positive control C48/80 could cause cell degranulation,and most of the cells were deeply stained. There was significant difference in positive cell rate between different batches of safflower yellow and positive control group. In the mice model for acute anaphylactoid reaction,it was found that the positive control C48/80 significantly increased the histamine content in the plasma of mice,while the safflower yellow in each batch did not cause a significant increase in plasma histamine( P<0. 000 1). The mechanism of anaphylactoid reaction is relatively complicated. This study was mainly based on the release of histamine and other active substances by degranulation of mast cells. No significant degranulation reaction of RBL-2 H3 cells induced by safflower yellow for injection was detected,nor was the plasma histamine level significantly increased in mice from the in vitro and in vivo aspects.

Protective cerebrovascular effects of hydroxysafflor yellow A (HSYA) on ischemic stroke.

The purpose of the present work was designed to explore protective cerebrovascular effects of hydroxysafflor yellow A (HSYA), and provide preclinical efficacy and mechanism data for its possible application in patients with cerebral ischemia. The protective effect of HSYA on ischemic stroke was evaluated by infarct sizes and neurological scores in Sprague-Dawley (SD) rats with middle cerebral artery occlusion (MCAO). Cerebrovascular permeability was detected by Evans blue dye leakage in MCAO rats. Cerebral blood flow, as well as blood pressure and heart rate were monitored using flow probes in Beagle dogs. Basilar artery tension isolated from Beagle dogs was evaluated with an MPA 2000 data-acquisition system. Coagulation-related function was also judged, including rabbit platelet aggregation by adenosine diphosphate (ADP) and platelet-aggregating factor (PAF), rabbit blood viscosity by a blood viscometer, and thrombus formation by rat arterial-venous shunts. Results showed that HSYA treatment significantly decreased the infarct sizes, neurological scores and cerebrovascular permeability in rats with MCAO. However, cerebral blood flow, blood pressure and heart rate were not affected by HSYA. In vitro, HSYA had a strong effect on cerebrovascular vasodilatation, and significantly decreased platelet aggregation, blood viscosity, and thrombogenesis. Besides well-known anti-coagulation effects, HSYA protects against ischemic stroke by dilating cerebral vessels and improving cerebrovascular permeability.

[Effects of different treatment methods of housefly pupae for the reproduction of Pachycrepoideus vindemmiae Rondani].

It is an important way to massively rear parasitoid wasps by using appropriate methods to treat the wasps' hosts and preserve them for a long duration. Pachycrepoideus vindemmiae Rondani is a pupal parasitoid of several dipteral pests, being of significance for the biological control of the pests. In this paper, housefly pupae were frozen at -20 degrees C, cold storage-preserved at 6 degrees C, and CO2-asphyxiated for 1-, 3-, and 30 days, respectively, and some pupae were heat-killed and cold storage-preserved for 30 days, aimed to approach the effects of these treatment methods on the reproduction of P. vindemmiae on the pupae. The results showed that P. vindemmiae could reproduce on the pupae treated with the above-mentioned methods, and the tibia length of the offspring had less difference with that on the fresh pupae. However, the reproduction of P. vindemmiae on the pupae treated with the above-mentioned methods except frozen decreased with the increasing preserving duration of the pupae. At the prerequisite of preserving for 30 days, frozen pupae had the highest P. vindemmiae offspring reproduction, suggesting that P. vindemmiae could be massively reared when the housefly pupae were treated by frozen and cold storage-preserved.

Defects in NKG2D ligand expression result in failed tolerance induction at the maternal-fetal interface: a possible cause for recurrent miscarriage.

Certain maternal immune responses against the fetus at the maternal-fetal interface may contribute to recurrent miscarriage (RM). Trophoblast cells involve in forming of maternal-fetal interface and interact with many immune cells, including NK cells. NK cells accumulate at the maternal-fetal interface and play a critical role during pregnancy. NKG2D ligands can activate NK cells through engaging with corresponding receptors. The 5'-end flanking regions of DNA sequence of some NKG2D ligands contain heat shock elements. It is very possible that oxidative stress, produced in pathological process of RM, induces abnormal NKG2D ligand expression in the trophoblast cells, which stimulate cytotoxicity of NK cells. Moreover, in normal pregnancy, soluble NKG2D ligands are secreted into sera by syncytiotrophoblast cells, which disturb NKG2D-mediated maternal anti-fetus immunity. Reduction of soluble NKG2D ligand levels in association with upregulation of NKG2D on immune cells may also contribute to pathogenesis of RM.