Objective To analyze the risk factors for meconium-stained amniotic fluid(MSAF)in preterm infants and the clinical outcome and prognosis of preterm infants.Methods Preterm infants with gestational age＜37 weeks delivered in Zhangjiajie People's Hospital from January 2022 to December 2023 were used as the study subjects,31 cases with MSAF were in MSAF group,and 31 cases of preterm infants hospitalized during the same period without MSAF were randomly paired in the ratio of 1∶1 to select with gestational age-body mass matching as non-MSAF group.Retrospective collection and analysis of pregnancy and perinatal conditions of mothers of preterm infants in two groups,comparing the differences of related factors between two groups of children;Logistic regression analysis of risk factors related to MSAF in preterm infants;comparing the complications and clinical outcomes of preterm infants in two groups.Results A total of 387 preterm infants with gestational age＜37 weeks were collected during the study period,including 31 preterm infants with comorbid MSAF,and the prevalence of MSAF in preterm infants was 8.0％.MSAF group had a higher incidence of advanced maternal age,premature rupture of membranes＞18 hours,antepartum fever,and cholestasis during pregnancy than non-MSAF group.Logistic regression analysis suggested that combined cholestasis during pregnancy and white blood cell count ≥ 30× 109/L within 6 hours after birth increased the incidence of MSAF in preterm infants.There was no statistically significant difference in the results of postnatal umbilical artery blood gas analysis between two groups of preterm infants.The proportion of leukocyte count ≥30×109/L,ultrasensitive C-reactive protein＞0.8 mg/L,and interleukin 6＞6 pg/L in MSAF group was higher than that of non-MSAF group in the 6 hours after birth.MSAF group had a higher incidence of intrauterine infectious pneumonia,feeding intolerance,and necrotizing small bowel colitis in neonates than non-MSAF group.Conclusion Advanced maternal age,intrauterine infections,and combined intrahepatic cholestasis during pregnancy may be the major risk factors for MSAF in preterm infants.MSAF preterm infants have a higher prevalence of intrauterine infectious pneumonitis,feeding intolerance,and necrotizing small bowel colitis in newborns,as well as longer hospital stays.

Objective:To investigate the effects and mechanisms of cyclic adenosine monophosphate (cAMP) on cisplatin-induced acute kidney injury (AKI).Methods:GSE227970 dataset derived from human renal tubular epithelial cells (HK-2 cells) in the GEO database was downloaded, and Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analysis were performed in normal and cisplatin-damaged cells. Eighteen 8-week-old male C57BL/6J mice with body weight of (22±2) g were randomly divided into normal group, cisplatin group and cAMP group according to random number table method, with 6 mice in each group. cAMP group was intraperitoneally injected with 30 mg/kg glumine cyclic adenosine monophosphate, while normal group and cisplatin group were intraperitoneally injected with the same volume of 0.9% sodium chloride solution for 10 consecutive days. The cisplatin and cAMP groups were intraperitoneally injected with 20 mg/kg cisplatin once on the 8th day. The body weight and kidney weight of mice were weighed, and kidney weight to body weight ratio was calculated. The blood urea nitrogen (BUN) and serum creatinine (Scr) in mice were detected. HE staining was used to evaluate the degree of renal injury. Western blotting was used to detect the protein expression of AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) signaling pathway in renal tissues. In vitro experiments, HK-2 cells were set up in normal group, cisplatin group, cAMP group and cAMP+AMPK inhibitor group. Immunofluorescence was used to detect the protein expression of phosphorylated (p)-AMPK in HK-2 cells. Adenosine triphosphate content and ratio of NAD + to NADH in cells were detected. Flow cytometry was used to detect cell apoptosis. Results:Biological signal analysis showed that axon guidance, Ras-related protein 1 signaling pathway and cAMP signaling pathway were significantly changed in cisplatin group. The body weight, kidney weight and kidney weight/body weight ratio in cisplatin group were significantly lower than those in normal group (all P<0.05). However, after cAMP treatment, kidney weight was significantly higher compared with cisplatin group ( P<0.05), and body weight and kidney weight/body weight ratio also increased, but the differences were not statistically significant (both P>0.05). BUN, Scr and renal tubular injury score in cisplatin group were significantly higher than those in normal group (all P<0.05). After cAMP treatment, BUN, Scr and renal tubular injury score were significantly lower than those in cisplatin group (all P<0.05). Western blotting results showed that cAMP treatment could significantly increase the decreased AMPK/ACC signaling pathway protein in the renal tissues of cisplatin-induced mice (all P<0.05). In vitro experiments, immunofluorescence detection showed that the expression of p-AMPK protein in cisplatin-induced HK-2 cells decreased, and the addition of cAMP increased the expression of p-AMPK protein in cisplatin-induced HK-2 cells (all P<0.05). cAMP treatment could alleviate cisplatin-induced injury in HK-2 cells, restore the reduction of adenosine triphosphate content and NAD +/NADH ratio, and reduce the apoptosis induced by cisplatin (all P<0.05), while AMPK inhibitor could eliminate the protective effect of cAMP on cisplatin-induced injury in HK-2 cells. Conclusion:cAMP can play a protective role in renal injury caused by cisplatin, and its mechanism may be related to activation of AMPK/ACC signaling pathway.

Aim To investigate the anti-acute lung injury(ALI)effect of Sterculiae Lychnophorae Semen(SLS)and its mechanism.Methods The main ac-tive components of SLS and their core targets and path-ways of action against ALI were obtained by network pharmacology methods.Subsequently,molecular doc-king technology and in vitro cellular experiments were applied for validation.Results A total of 19 core tar-gets were obtained,including HSP90AA1,CASP3,TNF,MAPK8 and MAPK14.The mechanisms may in-volve signaling pathways such as cancer,PI3K/Akt and MAPK.Molecular docking confirmed that the key targets of SLS formed a better binding activity with the relevant active ingredients.The in vitro results showed that SLS was able to protect the PM2.5-contaminated BEAS-2B cells,inhibit their NO,IL-1β and TNF-αlevels,and reduce the expression of p-p38 MAPK and p-JNK proteins.Conclusions The study successfully predicts the active ingredients,targets and signaling pathways of SLS against ALI,and in vitro experiments demonstrate that SLS might protect BEAS-2B cells from PM2.5 stimulus-induced inflammation and apoptosis by inhibiting the over-activation of p38 MAPK and JNK signaling pathways.

Ecological cultivation is an important way for the sustainable production of traditional Chinese medicine in the context of the carbon peaking and carbon neutrality goals. Facility cultivation and simulative habitat cultivation modes have been developed and applied to develop the endangered Dendrobium huoshanense on the basis of protection. However, the differences in the greenhouse gas emissions and global warming potential of these cultivation modes remain unexplored, which limits the accurate assessment of carbon-friendly ecological cultivation modes of D. huoshanense. Greenhouse gas emission flux monitoring based on the static chamber method provides an effective way to solve this problem. Therefore, this study conducted a field experiment in the facility cultivation and simulative habitat cultivation modes at a D. huoshanense cultivation base in Dabie Mountains, Anhui Province. From April 2023 to March 2024, samples of greenhouse gases were collected every month, and the concentrations of CO_2, CH_4, and N_2O of the samples were then detected by gas chromatography. The greenhouse gas emission fluxes, cumulative emissions, and global warming potential were further calculated, and the following results were obtained.(1)The two cultivation modes of D. huoshanense showed significant differences in greenhouse gas emission fluxes, especially the CO_2 emission flux, with a pattern of facility cultivation>simulative habitat cultivation [(35.60±11.70)mg·m~(-2)·h~(-1) vs(2.10±4.59)mg·m~(-2)·h~(-1)].(2) The annual cumulative CO_2 emission flux in the case of facility cultivation was significantly higher than that of simulative habitat cultivation[(3 077.00±842.00)kg·hm~(-2) vs(221.00±332.00)kg·hm~(-2)], while no significant difference was found in annual cumulative CH_4 and N_2O emission fluxes.(3) The facility cultivation mode had a significantly higher global warming potential than the simulative habitat cultivation mode [(3 053.00±847.00)kg·hm~(-2) vs(196.00±362.00)kg·hm~(-2)]. Overall, the simulative habitat cultivation of D. huoshanense has obvious carbon-friendly characteristics compared with facility cultivation, which is in line with the concept of ecological cultivation of medicinal plants. This study is of great reference significance for the implementation and promotion of the ecological cultivation mode of D. huoshanense under carbon peaking and carbon neutrality goals.
Dendrobium/chemistry* ; Greenhouse Gases/metabolism* ; Carbon/analysis* ; Ecosystem ; Carbon Dioxide/metabolism* ; China ; Global Warming

Aim To explore the effect of hydroxysafflor yellow A(HSYA)on lipocalin 2(LCN2)-induced fer-roptosis in HT22 cells and the related mechanism.Methods Thirty male Sprague-Dawley(SD)rats were used to establish the middle cerebral artery occlu-sion/reperfusion(MCAO/R)model by the suture method.The rats were randomly divided into the Sham group,the MCAO/R group,and the MCAO/R+HSYA group.The infarct area was measured by TTC staining,and the degree of neurological deficit was evaluated by the Z-Longa scoring method.The expressions of LCN2 and 24P3R in brain tissues were detected by Western blot.LCN2 protein was added to HT-22 cells,and the cells were divided into the normal group,the LCN2 group,and the LCN2+HSYA group.The optimal con-centration of LCN2-induced neuronal ferroptosis was screened by LDH assay and Western blot,and the ex-pression levels of ferritin,FPN1,GPX4,SLC7A11,COX2,and 24P3R were detected.LCN2 was knocked down by siRNA transfection,and the expressions of GPX4 and ferritin were detected.The contents of glu-tathione(GSH),malondialdehyde(MDA),GPX4,and Fe2+were determined by colorimetry,and the expres-sion of GPX4 was detected by immunofluorescence.The binding force between HSYA and LCN2 was ana-lyzed by molecular docking technology.Results Ani-mal experiments showed that HSYA could reduce the cerebral infarction area and decrease the neurological function score of MCAO/R rats.Compared with the sham group,the levels of LCN2 and 24P3R increased in the MCAO/R group,while HSYA inhibited their ex-pressions.Cell experiments showed that the optimal concentration of LCN2 to induce ferroptosis in HT22 cells was 2 μmol·L-1.After knocking down LCN2 by siRNA transfection,compared with the LCN2 group,the expression levels of GPX4 and ferritin in the siLCN2 group increased significantly.Compared with the nor-mal group,the expressions of SLC7A11,GPX4,FPN1,ferritin,and GSH in the LCN2 group decreased signifi-cantly,while the concentration of Fe2+,and the expres-sions of MDA,COX2,and 24P3R increased.HSYA could increase the expressions of SLC7A11,GPX4,FPN1,ferritin,and GSH,reduce the contents of Fe2+and MDA,and inhibit the expressions of COX2 and 24P3R.Molecular docking showed that the binding en-ergy between HSYA and LCN2 was-8.0 kJ·mol-1.Conclusion HSYA can inhibit LCN2-induced ferrop-tosis in HT22 cells through the SLC7A11/GPX4 signa-ling pathway.

Aim To explore the effect of hydroxysafflor yellow A(HSYA)on lipocalin 2(LCN2)-induced fer-roptosis in HT22 cells and the related mechanism.Methods Thirty male Sprague-Dawley(SD)rats were used to establish the middle cerebral artery occlu-sion/reperfusion(MCAO/R)model by the suture method.The rats were randomly divided into the Sham group,the MCAO/R group,and the MCAO/R+HSYA group.The infarct area was measured by TTC staining,and the degree of neurological deficit was evaluated by the Z-Longa scoring method.The expressions of LCN2 and 24P3R in brain tissues were detected by Western blot.LCN2 protein was added to HT-22 cells,and the cells were divided into the normal group,the LCN2 group,and the LCN2+HSYA group.The optimal con-centration of LCN2-induced neuronal ferroptosis was screened by LDH assay and Western blot,and the ex-pression levels of ferritin,FPN1,GPX4,SLC7A11,COX2,and 24P3R were detected.LCN2 was knocked down by siRNA transfection,and the expressions of GPX4 and ferritin were detected.The contents of glu-tathione(GSH),malondialdehyde(MDA),GPX4,and Fe2+were determined by colorimetry,and the expres-sion of GPX4 was detected by immunofluorescence.The binding force between HSYA and LCN2 was ana-lyzed by molecular docking technology.Results Ani-mal experiments showed that HSYA could reduce the cerebral infarction area and decrease the neurological function score of MCAO/R rats.Compared with the sham group,the levels of LCN2 and 24P3R increased in the MCAO/R group,while HSYA inhibited their ex-pressions.Cell experiments showed that the optimal concentration of LCN2 to induce ferroptosis in HT22 cells was 2 μmol·L-1.After knocking down LCN2 by siRNA transfection,compared with the LCN2 group,the expression levels of GPX4 and ferritin in the siLCN2 group increased significantly.Compared with the nor-mal group,the expressions of SLC7A11,GPX4,FPN1,ferritin,and GSH in the LCN2 group decreased signifi-cantly,while the concentration of Fe2+,and the expres-sions of MDA,COX2,and 24P3R increased.HSYA could increase the expressions of SLC7A11,GPX4,FPN1,ferritin,and GSH,reduce the contents of Fe2+and MDA,and inhibit the expressions of COX2 and 24P3R.Molecular docking showed that the binding en-ergy between HSYA and LCN2 was-8.0 kJ·mol-1.Conclusion HSYA can inhibit LCN2-induced ferrop-tosis in HT22 cells through the SLC7A11/GPX4 signa-ling pathway.