Acute kidney injury (AKI) is a critical clinical condition characterized by rapid renal function decline, with high morbidity, mortality, and healthcare costs. Traditional Chinese medicine (TCM) has shown potential effects on mitigating oxidative stress and programmed cell death in AKI models. Scutellaria barbata D. Don (SB) and Scleromitrion diffusum (Willd.) R. J. Wang (SD), a classic TCM herbal pair exhibited anti-inflammatory and antioxidant activities. Using advanced chromatographic separation technology, we enriched the effective fractions of water extracts from SB-SD, obtaining self-assembled herbal nanoparticles (SB and SD nanoparticles, SSNPs) rich in flavonoids and terpenoids. These SSNPs demonstrated robust antioxidant properties in vitro and mitigated AKI progression in vivo by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. Oral administration of SSNPs in mice resulted in absorption into the bloodstream, formation of a protein corona, reduced macrophage phagocytosis, and enhanced bioavailability and renal targeting. Furthermore, we investigated the self-assembly principle of SSNPs using representative flavonoids and terpenoids. Kinetic studies and in situ transmission electron microscopy (in situ TEM) revealed that these compounds self-assemble via supramolecular forces like hydrogen bonding and π-π interactions, forming stable nanostructures. This study elucidates the renoprotective effects and mechanisms of SB and SD, and provides a novel approach for the development of TCM-based nanomedicines, highlighting the potential of nano-TCM in AKI treatment.

Objective:To analyze the status quo, hotspots and fronts of emergency nursing training research at home and abroad in the past ten years, and to provide reference and ideas for the efficient development of emergency nursing training in China.Methods:CiteSpace 6.2.R2 software was used to visually analyze the Chinese and English literatures on emergency nursing training included in CNKI and Web of Science core databases from January 1, 2013 to June 1, 2023.Results:A total of 1 177 Chinese literatures and 1 163 English literatures were included. The number of foreign articles in this field increased year by year, while the number of domestic articles showed a downward trend since 2018. There were many stable core author groups and core institution groups in foreign countries, while there was less cooperation among domestic authors and institutions. The common research hotspots and frontiers at home and abroad focused on broadening the training audience of emergency nursing, innovating the training methods of emergency nursing, strengthening the evaluation of the effect of emergency nursing training, and paying attention to the training experience and needs of nurses. Foreign researches also focused on specialized nurses, interprofessional education and nurses′mental health, etc, and the research direction was diversified.Conclusions:The development stages of emergency nursing training researches at home and abroad are different, and the research hotspots are different. In the future, we should learn from foreign research, strengthen interdisciplinary cooperation, improve the depth and breadth of research, and strengthen the cooperation between authors, institutions and countries to promote the high-quality development of emergency nursing training research in China.

ObjectiveTo explore the molecular mechanism of Shuyuwan regulating polarization of tumor-associated macrophages （TAMs） to inhibit the progression of colorectal cancer （CRC）. MethodThe nude mouse model of orthotopic transplantation of colon cancer was established. Male BALB/c-nu nude mice （n=28， 4 weeks old） were randomly assigned into 4 groups （n=7）： Model group （normal saline） and low-， medium-， and high-dose （1.725， 2.310， 2.895 g·kg^-1·d^-1， respectively） Shuyuwan groups. On day 9 after the tumor block was inoculated， the mice were administrated by gavage with corresponding agents at a dose of 15 mL·kg^-1 once a day， 6 days a week， and no agent on the 7^th day. After two consecutive weeks of intervention， the nude mice were sacrificed and the tumor samples were collected. A part of the colon tissue and the tumor tissue was used to prepare sections， and hematoxylin-eosin （HE） staining was performed for pathological observation. The expression of inducible nitric oxide synthase （iNOS） and arginase-1 （Arg-1） in the tumor tissue was detected by immunohistochemistry （IHC）. The mRNA levels of interleukin-12 （IL-12）， epidermal growth factor （EGF）， and transforming growth factor-β₁ （TGF-β₁） in the tumor tissue were determined by Real-time polymerase chain reaction （PCR）. Western blot was employed to determine the protein levels of iNOS， IL-12， EGF， and TGF-β₁ in the tumor tissue. ResultCompared with the model group， Shuyuwan inhibited the growth of colon cancer cells in nude mice and caused the tumor cell necrosis in different degrees. The high-dose Shuyuwan group had the strongest inhibitory effect on the growth of tumor cells， which basically lost the normal morphology. Furthermore， Shuyuwan up-regulated the expression of iNOS and IL-12 in M1-type macrophages （P<0.05） and down-regulated the expression of Arg-1， EGF， and TGF-β₁ in M2-type macrophages （P<0.05）， which indicated the weakened polarization of macrophages toward M2 type and the enhanced polarization toward M1 type after treatment with Shuyuwan. ConclusionShuyuwan can inhibit the growth of orthotopically transplanted colon tumor by blocking the polarization of TAMs to M2 type and promoting the polarization of TAMs to M1 type.

Aim To investigate the effect of magnesi-um isoglycyrrhizinate (MgIG)on radiation -induced pulmonary fibrosis in mice and the mechanism.Meth-ods Fifty female C57BL/6 mice were randomly divid-ed into control group,irradiation (RT)group,MgIG group,RT +MgIG group and RT +dexamethasone (DXM)group,with 1 0 mice in each group.Except for control group and MgIG group,the remaining mice were given a single 1 5Gy 60 Co γray on whole lung. The mice in each group were administered 2 h before irradiation and each day after irradiation:MgIG group and RT +MgIG group were administered with MgIG (1 00 mg·kg -1 )by intraperitoneal injection;control group and RT group were administered with normal sa-line (20 mL·kg -1 )by intraperitoneal injection;RT+DXMgroup was administered with DXM(0.5 mg· kg -1 )by intraperitoneal injection.After 1 2 weeks,the mice were sacrificed and lung tissues were taken out. The degree of alveolitis and pulmonary fibrosis were observed by HE staining and Masson staining.The ex-pressions of type Ⅰ collagen,type Ⅲ collagen and TGF-β1 protein were detected by immunohistochem-isty.Results The alveolitis,pulmonary fibrosis and expressions of type Ⅰ collagen,type Ⅲ collagen, TGF-β1 ,p-Smad2,p-Smad3 increased significantly in RT group compared with control group (P <0.05 ), and were significantly lower in RT +MgIG group and RT +DXMgroup than those in RT group(P <0.05). Conclusion MgIG can improve radiation-induced pulmonary fibrosis in mouse lung tissue,and its mech-anism may be related to the influence of MgIG on TGF-βsignaling pathway.

Aim To establish primary cultured rat hip-pocampal neuron damage model induced by aluminum maltolate and study the effect of intervention for DP2 on primary cultured rat hippocampal neuron treated with aluminum overload. Methods The hippocampus was dissected out from fetal rat ( embryonic 18 d ) . After being cultured for 7 d, the hippocampal neuron was treated with Al( malt) 3 to establish the model of prima-ry cultured rat hippocampal neuron damage and mean-while treated with DP2 agonist DK-PGD2 and DP2 an-tagonist CAY10471, respectively. After treatment for 24 h, the cell viability was measured by MTT and LDH, Ca2+ fluorescence intensity. Neuronal pathomor-phology was observed by HE staining. Results The purity of hippocampal neuron was more than 95%. Compared with the control group, the number of hipp-ocampal neurons was reduced and neurons became chromatic agglutination and karyopyknosis in aluminum overload group. Treatment of aluminum caused a sig-nificant decrease in MTT value ( P<0. 01 ) and an in-crease in the LDH leakage rate (P<0. 01). The Ca2+fluorescence intensity significantly increased ( P <0. 01 ) in aluminum overload group. Compared with that of the aluminum overload group, treatment of DK-PGD2 , a selective DP2 agonist, significantly aggravated the primary cultured rat hippocampal neuron injury caused by aluminum overload accompanied with the significant decrease of MTT value ( P <0. 01 , P <0. 05 ) and an increase of the LDH leakage rate ( P<0. 01), significant increase of Ca2+ fluorescence inten-sity of neuron. Treatment of CAY10471, a selective DP2 antagonist, had opposite effects of DK-PGD2 . Conclusion The activation of DP2 can increase hipp-ocampal neural susceptibility to aluminum overload.

Objective To study the expressions of miR-10a, miR-93 and miR-200a in malignant ovarian tumor tissues and their clinical significances.Methods Real-time quantitative PCR was used to detect the expression of 40 cases of normal ovarian tissue, 40 cases of benign ovarian cyst and 40 cases of miR-10a, miR-93 and miR-200a in malignant ovarian tumor tissues.Analysis of variance and t-Test were respectively applied to compare the expression of miR in different tissues and analyze the correlation between miR and clinicopathological characteristics of malignant ovarian tumor .Kaplan-Meier Log-rank test and Cox proportional hazards regression model were adopted in prognosis.Results The expression lev-els of miR-10a in ovarian cancer tissues were significantly higher than that in benign ovarian tumor tissues and normal ovari-an tissues (p<0.001), whereas the expression of miR-93 and miR-200a in the three types of tissues was no statistically significant difference (p>0.05).The expression quantity of miR-10a in malignant ovarian tumor tissues with greater omen-tum metastasis, lymph node metastasis and distant organ metastasis was significantly higher than that without metastasis ( p<0.05).The median survival time of patients with higher expression of miR -10a was lower than that of patients with low ex-pression of miR-10a (p=0.01).Multi-factor Cox model analysis showed that the expression quantity of miR -10a was an independent factor affecting survival prognosis in patients(p=0.002).Conclusion Our data suggest that miR-10a is asso-ciated with ovarian cancer metastasis, which is the main factor affecting prognosis in ovarian cancer.It might serve as a bio-marker for judging the prognosis in ovarian cancer.

Aim To investigate the protective effects of beraprost sodium on cerebral cortical neuron injury in chronic aluminum-overload rats and its effects on PGIS-IP signaling pathway. Methods 75 SD rats were randomized into five groups: normal control group, chronic aluminum-overload group ( model group) and beraprost sodium groups-low dose (6 μg· kg-1 ), medium dose ( 12 μg · kg-1 ) and high dose (24 μg·kg-1). Aluminum gluconate (Al3+ 200 mg ·kg-1 d-1, once a day, 5d a week, for 20 weeks, p. o. ) was administered to rats of cerebral damage model. The rats of experimental groups were concomi-tantly treated with beraprost sodium ( p. o. ) daily for 20 weeks. After the model was built successfully, the spatial learning and memory( SLM) function was done by Morris water maze. The cortical neurons damage was detected by HE staining, SOD activities and MDA contents. The 6-k-PGF1α levels in cortex were meas-ured by ELISA. The expressions of PGIS, IP mRNA and IP protein were also studied. Results Compared with the rats of normal control group, the SLM function was significantly impaired ( P<0. 01 ) and considera-ble karyopycnosis was observed in model group rats. The SOD activities were weakened ( P <0. 01 ), the MDA contents increased ( P<0. 05 ) and the levels of 6-k-PGF1α raised significantly ( P <0. 01). The ex-pressions of PGIS and IP mRNA in the rats cortex obvi-ously increased ( P<0. 01 ), so did the expression of IP protein(P<0. 05). Compared with the rats of mod-el group, the SLM function of rats in experimental groups decreased significantly ( P<0. 01 ) and damage of cortical neurons reduced remarkably. The SOD ac-tivities increased ( P <0. 01 ) and the MDA contents decreased ( P <0. 01). Besides, the content of 6-k-PGF1α, the expressions of PGIS mRNA and IP protein in the rats cortex decreased significantly ( P<0. 05 ) as well as IP mRNA ( P<0. 01). Conclusion Our re-sults demonstrate that in cerebral cortical neuron of chronic aluminum-overload rats, beraprost sodium has notably protective effects and the mechanism might be related to PGIS-IP signaling pathway.

Objective To retrospectively analyze the relationship between benign prostatic hyperplasia (BPH) and metabolic syndrome (MS) in senior patients. Methods The 859 male senior patients including 619 cases with BPH and 8 cases with MS were enrolled in this study, and there were 192 cases with both diseases and 40 controls. The levels of fasting blood glucose (FBG), total cholesterol (TC), triacylglycerol (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were measured. The body mass index (BMI), prostate volume and annual prostate growth rate were determined or calculated. The correlations of BPH with other metabolic risk factors were analyzed. Results The levels of systolic blood pressure (SBP), diastolic blood pressure (DBP), body weight, BMI, TG and FPG were higher (t=6.15, 5.99, 13.12, 15.56, 10.63 and 9.94, all P＜0.01), while serum HDL-C level was lower (t=-7.57,P＜0.01) in BPH patients with MS than without MS. As the number of components of MS was increased, the prostate volume was increased (F=2.98, P=0.031). As the age, body weight, BMI, SBP and PG were increased, the prostate volume was increased (t=-6.39,-2.39,-2.36,-2.13,-25.85,all P＜0.05). Spearman analysis showed that prostate volume was positively correlated with age, SBP, body weight, BMI and hypertension (r=0.229, 0.079, 0.090, 0.089 and 0.088, all P＜0.05). And age, body weight and SBP were the independent risk factors for BPH (OR=1.07, 1.03 and 1.34, all P＜0.05). Conclusions The present study demonstrates a relationship between BPH and MS in senior patients. Future studies are needed to confirm our results and to explain underlying mechanisms.

OBJECTIVETo study the anti-cancer effect of matrine (Mat) on U937 cell line and its possible molecular mechanism.

METHODThe cells were cultured in medium containing either 0.1, 0.2, 0.3, 0.4, or 0.5 g x L(-1) of Mat. The morphological alteration was observed by inverted microscopy and electron microscopy. Cell proliferation was analyzed by Try pan blue staining and MTT. The method of Western Blot was used to detect phosphorylation activity of MAPK.

RESULTMatrine had a significant inhibitory effect on proliferation of U937 cell line at the concentration of 0.2 g x L(-1). Treated with matrine of 0.2 g x L(-1) for 48 h, U937 cells became smaller and appeared more round than previously. The number of U937 cells showing apoptosis increased with elevation of the concentration of the matrine. Matrine had an ability of inhibiting the activity of ERK and increasing the activities of p38 and JNK to some degree in U937 cells.

CONCLUSIONMatrine can inhibit the proliferation of U937 cell line in vitro and induce its apoptosis possibly through inhibiting the activity of ERK and increasing the activities of p38 and JNK in U937 cells.

Alkaloids ; pharmacology ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Humans ; MAP Kinase Signaling System ; drug effects ; Quinolizines ; pharmacology ; U937 Cells

OBJECTIVEThe objective of this paper was to study the change of P38MAPK and Fas in the apoptosis of THP-1 cells induced by allicin.

METHODThe proliferation inhibition rates of THP-1 cells after various treatments were examined by MTT assay. Apoptosis rate was determined with Annexin V- FITC/PI double staining by flow cytometry. The expression and distribution change of the phosphorylation p38MAPK (P-p38MAPK) were detected by immunohistochemical staining. The changes of P-p38 MAPK and Fas proteins were detected by Western blot.

RESULTThe proliferations of leukemia cell line THP-1 are inhibited by allicin. MTT assay showed that allicin can inhibit the proliferation of the THP-1 cell, and the inhibition was dependent on both dose and time. The IC50 of 72 hours was 12.8 mg x L(-1). Apoptosis rate detected by Annexin V-FITC/PI was proportional to the concentration of the allicin. After the immunohistochemical staining test, the P-p38MAPK was located in the cell nucleus and plasma, showing deep brown, when adding allicin to THP-1 cell. Western blot test showed that the P-p38MAPK proteins expression was proportional to the concentration of Allicin and was also dose dependent. The levels of P-p38MAPK in negative control group, 1/2 IC50 of 72 hours group and IC50 of 72 hours group were 0.259 8 +/- 0.013 2, 0.61 2 +/- 0.008 3 and 0.505 6 +/- 0.005 5 respectively, and the levels of Fas proteins were 0.287 4 +/- 0.008 9, 0.426 8 +/- 0.007 9 and 0.597 1 +/- 0.010 9 respectively. The difference was statistically significant when compared with the negative control group (P < 0.01).

CONCLUSIONAllicin can significantly induce THP-1 cells apoptosis, and its mechanism may be related to the activation of P38MAPK/Fas.

Apoptosis ; drug effects ; Cell Line, Tumor ; Humans ; Neoplasms ; drug therapy ; metabolism ; physiopathology ; Phosphorylation ; Signal Transduction ; drug effects ; Sulfinic Acids ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; genetics ; metabolism