Objective To explore the effect of laparoscopic salpingectomy on ovarian reserve function and serum neuropeptide Y(NPY)and cortisol(Cor)in patients with ectopic pregnancy.Methods 82 patients with ectopic pregnancy who had visited Chaohu Hospital Affiliated to Anhui Medical University from June 2018 to June 2021 were randomly divided into two groups,with 41 in each group.The control group underwent laparoscopic salpingostomy and suturing for embryo retrieval,while the study group underwent laparoscopic salpingectomy.Surgical duration,intraoperative blood loss,time to postsurgical mobilization,length of hospital stay,serum NPY and Cor levels,antral follicle count(AFC),indexes for peak flow velocity and resistance of ovarian artery were compared between the two groups.Follow-up was conducted for two years after surgery,and the success rate of pregnancy and the ectopic pregnancy rate were recorded.Results The surgical duration in the study group was shorter than that in the control group(P<0.05).The differences in serum NPY and Cor values between the two groups immediately after surgery and at postoperative week one were not statistically significant(P>0.05).At postoperative months1 and 6,the peak flow velocity of the affected ovary was lower in the study group than in the control group,whereas the resistance index was higher(P<0.05).At postoperative month 6,both groups showed an increase in peak flow velocity and a decrease in resistance index(P<0.05).There were no statistically signifi-cant differences in AFC and the success rate of pregnancy between the two groups postoperatively(P>0.05).The ectopic pregnancy rate in the study group was lower than that in the control group(P<0.05).Conclusion As compared with laparoscopic salpingostomy,laparoscopic salpingectomy for ectopic pregnancy can also preserve postoperative ovarian antral follicle count(AFC),and it has greater advantage in reducing the risk of recurrent ectopic pregnancy after surgery.

OBJECTIVE To investigate the effect of arctiin （ARC）relieving lipopolysaccharide （LPS）induced inflammatory injury of human nasopharyngeal epithelial cells NP- 69. METHODS The effects of 24 h treatment of 0.000 1，0.001，0.01，0.1， 1.0，10 μmol/L ARC on the proliferation of NP-69 were determined by MTS method. After 0.01，0.1，and 1.0 μmol/L ARC was applied to NP- 69 for 24 h and NP- 69 was pre-treated with 0.01，0.1 and 1.0 μmol/L ARC for 24 h，and then stimulated with 1.0 μg/mL LPS for 24 h，scratch tests were used to detect cell migration in both experiments. LPS stimulated NP- 69 to establish an inflammation injury model. The levels of nitric oxide （NO），tumor necrosis factor α（TNF-α）interleukin-6（IL-6），and IL- 1β in cell supernatants were detected ，and mRNA and protein expression of zonula oecludens protein 1（ZO-1），β-defensin 3（BD3）， Janus kinase 1 （JAK1），signal transducer and activator of transcription 3 （STAT3） in cell supernatant were also detected. RESULTS Compared with normal group ，0.000 1，0.001，0.01，0.1，1.0，10 μmol/L ARC had no effect on the proliferation of NP-69 after 24 h treatment （P＞0.05）. ARC （0.1，1.0 μmol/L）could significantly promote the rate of cell migration （P＜0.05）. For the inflammatory injure of NP- 69 cells stimulated by LPS ，ARC（1.0 μmol/L）could significantly reduce the release of NO ， TNF-α and IL-6（P＜0.05），significantly increased mRNA and protein expression of ZO- 1 and BD 3 but decreased mRNA and protein expression of STAT 3（P＜0.01 or P＜0.05）. CONCLUSIONS ARC has the effect of reducing the inflammatory injury of NP-69 cells induced by LPS ，promoting the physical and immune defense ability of the nasal mucosa epithelial barrierunder inflammatory environment. The mechanism of action may be related to inhibiting IL- 6/JAK1/STAT3 signaling pathway.

Potassium 2-(1-hydroxypentyl)-benzoate (d,l-PHPB), a new drug candidate for ischemic stroke at the phase II clinic trial, has been shown to protect neurons by inhibiting oxidative injury and reducing neuron apoptosis in previous studies. But the mechanisms of d,l-PHPB remain to be studied. In this study, a neuron-astrocytes co-culture system was used to elucidate the roles of astrocytes in neuroprotection of d,l-PHPB under oxygen-glucose deprivation/reoxygenation (OGD/R) condition. Our data showed that d,l-PHPB reduced neuronal apoptosis in mono-culture system and this effect was enhanced in neuron-astrocyte co-culture system under the OGD/R condition. Meanwhile, d,l-PHPB obviously increased the levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), which were mainly secreted from astrocytes, in the co-culture system after OGD/R. The PI3K/AKT and ERK signaling pathways as well as the p-TRKA/B receptors were involved in the process. In addition, the levels of TNF-and IL-1secreted from astrocytes after OGD/R were markedly reduced after d,l-PHPB treatment, which was mainly due to the suppression of phosphorylated p38. In conclusion, the present study demonstrates that the neuroprotective effects of d,l-PHPB were improved by astrocytes, mainly mediated by increasing the release of BDNF/NGF and attenuating inflammatory cytokines.

The purpose of this study is to investigate the expression of major potassium channel subtypes in the brain of chronical mild stress (CMS) rats and reveal the effects of fluoxetine on the expression of these channels. Rats were exposed to a variety of unpredictable stress for three weeks and induced anhedonia, lower sucrose preference, locomotor activity and lower body weight. The protein expressions were determined by Western blot. CMS significantly increased the expression of Kv2.1 channel in frontal cortex but not in hippocampus, and the expression level was normalized after fluoxetine treatment. The expression of TREK-1 channel was also obviously increased in frontal cortex in CMS rats. Fluoxetine treatment might prevent this increase. However, the expression of Kv3.1 and Kv4.2 channels was considerably decreased in hippocampus after CMS, and was not affected by fluoxetine. These results suggest that different subtypes of potassium channels are associated with the pathophysiology of depression and that the therapeutical effects of fluoxetine may relate to Kv2.1 and TREK-1 potassium channels.