To investigate the therapeutic effects and safety of the combination of azithromycin (injection and granules) and montelukast sodium tablets on the treatment of Mycoplasma pneumoniae pneumonia (MPP) in children of different severity.

The children with MPP treated in our hospital were divided into control group and treatment group based on the treatment method. All children received intravenous infusion of azithromycin injection at a dose of 10 mg·kg^-1 qd for 5 days until body temperature returned to normal, followed by oral administration of azithromycin granules at the same dose for 3 days, then 4 days off, for a total course of 3 weeks. On this basis, the treatment group was additionally given montelukast sodium tablets, with a dose of 4 mg·d^-1 for children ≤5 years old, and 5 mg·d^-1 for children over 5 years old, for a total course of 3 weeks. According to the severity of MPP, patients were divided into mild MPP group and severe MPP group. After treatment, the clinical efficacy, NLRP3 inflammasome pathway-related indicators and small airway function indicators were compared between the two groups of children with different severity levels; multiple linear regression was used to analyze the correlation between NLRP3 inflammasome pathway-related indicators and small airway function; and generalized estimating equation (GEE) model was used to analyze the changes in NLRP3 inflammasome pathway-related indicators at different time points, in different groups, and with different severities.

This study included a total of 92 patients, with 46 cases in each group. Confounding factors were adjusted using propensity score matching (PSM), and after matching, 40 cases were included in each group, while 47 cases in mild MPP group and 33 cases in severe MPP group. The white blood cell count (WBC) in severe MPP and mild MPP groups were (10.82±1.59) and (10.06±1.47) ×10⁹·L^-1, C-reactive protein (CRP) were (19.45±8.94) and (8.67±4.08) mg·L^-1, interleukin-6 (IL-6) were (18.25±4.48) and (13.65±4.33) pg·mL^-1, and interleukin-10 (IL-10) were (6.70±1.89) and (5.26±1.35) pg·mL^-1. Comparisons of these indicators between subgroups showed statistically significant differences (all P<0.05). The effective treatment rates of children with mild MPP in treatment group and control group were 100.00% (22 cases/22 cases) and 88.00% (22 cases/25 cases), respectively; the effective treatment rates of children with severe MPP were 88.89% (16 cases/18 cases) and 60.00% (9 cases/15 cases), respectively. Comparisons between groups showed that these differences were statistically significant (all P<0.05). After treatment, the mild and severe MPP children in treatment group had NLRP3 mRNA levels of 0.89±0.11 and 1.11±0.10, apoptosis-associated speck-like protein (ASC) mRNA levels of 0.77±0.10 and 0.95±0.15, caspase-1 mRNA levels of 0.69±0.09 and 0.82±0.10; forced expiratory flow at 25% of the pulmonary volume (FEF25%) levels were (2.72±0.24) and (2.28±0.19) L·s^-1, forced expiratory flow at 50% (FEF50%) levels were (2.90±0.40) and (2.37±0.31) L·s^-1, forced expiratory flow at 75% (FEF75%) levels were (2.13±0.32) and (1.73±0.35) L·s^-1, all showing statistically significant differences (all P<0.05). Correlation analysis showed that in children with MPP, the NLRP3 inflammasome pathway-related indicators NLRP3, ASC and caspase-1 mRNA were all negatively correlated with small airway function indicators FEF25%, FEF50% and FEF75%, and the negative correlations were statistically significant (all P<0.001). GEE results indicated that the reduction in NLRP3 mRNA levels in treatment group was greater than that in control group. In mild MPP, the estimated values for treatment and control groups were -0.76 and -0.56, respectively; the reduction in ASC mRNA in treatment group was greater than in the control group, with estimated values of -0.56 and -0.26, respectively; the reduction in caspase-1 mRNA in treatment group was greater than in control group, with estimated values of -0.32 and -0.26, respectively, and all interaction terms were statistically significant (all P<0.05).

Azithromycin combined with montelukast sodium can significantly improve the clinical efficacy of children with different severity of MPP, reduce the excessive inflammatory response of children with different severity of MPP by targeting and inhibit the NLRP3 inflammasome pathway, and improve the function of the small airway, especially in children with mild disease.

To observe the effectiveness and hepatorenal safety of Fule Cream alone or in combination with topical corticosteroids (TCS)/calcineurin inhibitors (TCI) in treating pediatric skin diseases.

Children prescribed Fule cream in our hospital were enrolled and categorized into monotherapy cohort (Fule Cream alone) and combination cohort (Fule cream with TCS/TCI) based on medication use. The changes in liver and kidney function indicators, the incidence of drug-induced liver injury (DILI), acute kidney injury (AKI) and clinical effectiveness were compared between the two cohorts. Outcome variables for effectiveness were constructed by extracting efficacy descriptions from medical record texts.

A total of 2 439 children were included for safety analysis and 741 for effectiveness analysis. Effectiveness analysis showed that the combination cohort had a significantly higher response rate of 77.93% (505 cases/648 cases) than the monotherapy cohort 56.99% (53 cases/93 cases) with an odds ratio (OR) of 0.38 (95% CI: 0.24-0.59). Regarding safety, after treatment, The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) in cohort 1 and cohort 2 were significantly decreased after treatment (all P<0.05). The incidence of DILI and AKI was low. Data quality analysis revealed a high missing rate for follow-up laboratory tests and a lack of standardized efficacy evaluations.

The Fule Cream combined with TCS/TCI regimen demonstrated not only superior effectiveness but also no increased clinically significant hepatorenal risk in a real-world setting. Although data missingness may affect the precision of effect estimates, sensitivity analyses support the robustness of the primary conclusions. These findings provide real-world evidence supporting the clinical use of Fule Cream and highlight the necessity of enhancing data governance to generate higher-quality real-world evidence.

To observe the clinical efficacy and safety of remimazolam injection combined with fentanyl injection in the induction of general anesthesia for pediatric laparoscopic hernia surgery.

The children who underwent elective laparoscopic hernia surgery in our hospital were divided into successful sedation group and failed sedation group according to whether laryngeal mask placement was completed under sedation remedy. Remimazolam injection was administered intravenously, using an initial dose of 0.3 mg·kg^-1 with a dose increment of 0.05 mg·kg^-1. The dose for the next patient was determined according to the modified Dixon sequential method. Patients who successfully underwent laryngeal mask insertion were included in the sedation success group, while those requiring additional intravenous propofol for sedation to complete laryngeal mask insertion were included in the sedation failure group. Remimazolam injection combined with fentanyl injection was calculated by modified Probit regression for the induction of half effective dose (ED₅₀) and 95% effective dose (ED₉₅) and its 95% confidence interval (CI) in pediatric laparoscopic hernia induction of general anesthesia. Recorded vital signs during anesthesia induction, preoperative, dosage and intraoperative procedures, and evaluated for safety.

A total of 42 children who were planned for laparoscopic hernia surgery were screened in this study, of which were excluded due to abnormal preoperative examination (4 cases), parental refusal to participate (2 cases) and difficult airway (1 case), and finally, 35 hospitalized children who met the criteria were included. All enrolled children successfully completed the study process and no case dropped out, 18 cases of successful sedation and 17 cases of failed sedation. The ED₅₀ of remimazolam combined with fentanyl for general anesthesia induction in pediatric laparoscopic surgery was 0.22 mg·kg^-1, CI was (0.19~0.26), ED₉₅ was 0.32 mg·kg^-1, and CI was (0.28~0.51). The time from anesthesia induction to intubation in the successful and failed sedation groups were 4.58 (3.00, 5.00) and 4.63 (3.25, 5.75) min, respectively; the time of surgery were 13.63 (7.00, 17.00) and 14.00 (6.50, 18.00) min, respectively; the time from discontinuation to extubation were 17.84 (7.00, 21.00) and 16.50 (6.40, 22.75) min, respectively; and the stay time after resuscitation were 38.42 (30.00, 40.00) and 41.56 (22.10, 49.25) min, respectively. There was no significant difference between the above indicators in the successful sedation group and the failed sedation group (all P>0.05). The main adverse drug reactions in the successful sedation group were drowsiness, hypotension and hypoxemia, and in the sedation failure group were drowsiness and hypotension. The total incidence of adverse drug reactions in the successful sedation group and the failed sedation group were 22.22% (4 cases/18 cases) and 17.65% (3 cases/17cases). There was no significant difference between the above indicators in the successful sedation group and the failed sedation group (P>0.05).

The ED₅₀ of remimazolam combined with fentanyl for inserting a laryngeal mask in pediatric general anesthesia is 0.22 mg·kg^-1, with a CI of (0.19~0.26).

To observe the clinical efficacy and safety of combining nebulized budesonide suspension with microscopic support laryngoscope cool plasma radiofrequency ablation in the treatment of early glottic carcinoma (EGC).

EGC patients were divided into control group and treatment group based on different treatment regimens. Both groups underwent microscopic support laryngoscope cool plasma radiofrequency ablation. Postoperatively, the control group was administered oral cefaclor extended-release capsules at a dose of 0.5 g per time, twice daily, for 2 consecutive days. The treatment group was given inhaled budesonide suspension at a dosage of 1 mg for nebulization, twice a day, starting one week after surgery, and after one week, switched to nebulization with saline for 3 weeks based on control group. The clinical efficacy, laryngeal morphological indicators, objective voice acoustic indicators, voice disorder index and postoperative follow-up results were compared between the two groups, and conducted a safety assessment.

A total of 98 patients were included, 51 in control group and 47 in treatment group. After treatment, the overall effective rates for control and treatment groups were 84.31% (43 cases/51 cases) and 89.36% (42 cases /47 cases), respectively, with no statistically significant difference (P>0.05). At 4 weeks postoperatively, the morphological scores for the vocal folds in control and treatment groups were (1.45±0.73) and (1.13±0.74) points, respectively; the fundamental frequencies were (168.71±22.58) and (158.02±23.83) Hz, respectively; the frequency perturbations were (0.72±0.11)% and (0.67±0.13)% , respectively; the amplitude perturbations were (4.16±0.56)% and (3.89±0.47)%, respectively; the harmonic-to-noise ratios were (21.39±2.32) and (23.34±2.43) dB, respectively; the physiological scores were (18.45±2.89) and (17.00±3.16) , respectively, with all differences being statistically significant between the two groups (all P<0.05). One case of gastrointestinal reaction occurred in control group; one case of rash and two cases of gastrointestinal reaction occurred in treatment group. The total incidence of adverse drug reactions in treatment and control groups were 6.38% (3 cases/47 cases) and 1.96% (1 case/51 cases), respectively, with no statistically significant difference (P>0.05). The progression-free survival rates for control and treatment groups were 91.30% (42 cases/46 cases) and 95.45% (42 cases /44 cases), respectively, with no statistically significant difference (P>0.05).

Nebulized budesonide budesonide inhalation therapy combined with microscopic support laryngoscope cool plasma radiofrequency ablation provides comparable treatment efficacy to isolated microscopic support laryngoscope cool plasma radiofrequency ablation in patients with EGC, but the former demonstrates more significant improvement in vocal fold morphology and voice quality.

To evaluate the effects of centella asiatica acid (AA) on the apoptosis of cardiac microvascular endothelial cells (CMECs) and vascular regeneration by modulating the Toll-like receptor 4/myeloid differentiation primary response 88/nuclear factor kappa B/nucleotide-binding oligomerization domain-like receptor protein 3 (TLR4/MyD88/NF-κB/NLRP3) pathway.

The homocysteine (HCY)-induced rat CMECs were used to simulate and construct a coronary heart disease injury cell model, and the success of model construction was verified using the cell counting kit-8 (CCK8) method. The cells were divided into control group (normal culture), model group (modeling), centella asiatica acid group (modeling + 10 μmol·L^-1 AA) and combined group (modeling + 1 μg·mL^-1 lipopolysaccharide + 10 μmol·L^-1 AA). Cell viability was detected using CCK8, apoptosis was assessed by flow cytometry, and the relative expression levels of apoptosis-related proteins, pathway-related proteins and vascular regeneration-related proteins were measured by Western blot.

The cell viability of control group, model group, asiatica acid group and combination group were 0.92±0.01, 0.61±0, 0.75±0.01 and 0.50±0.02, respectively; the apoptosis rates were (4.96±0.53)%, (24.98±1.68)%, (18.22±0.96)% and (34.17±0.49)%, respectively; the relative protein expression levels of B-cell lymphoma/leukemia 2-associated X protein (Bax) were 0.12±0.01, 0.63±0, 0.42±0.02 and 0.96±0.01, respectively; the relative expression levels of Bcl-2 protein were 0.99±0.02, 0.34±0.01, 0.69±0.01 and 0.10±0.01, respectively; the relative expression levels of TLR4 protein were 0.19±0.01, 0.65±0, 0.41±0.01 and 0.84±0.01, respectively; the relative expression levels of Myd88 protein were 0.29±0.02, 0.77±0, 0.61±0.01 and 0.95±0.02, respectively; the relative expression levels of NF-κ B protein were 0.22±0.01, 0.82±0.02, 0.53±0.02 and 0.84±0.02, respectively; the relative expression levels of NLRP3 protein were 0.17±0.02, 0.75±0.03, 0.50±0.01 and 0.98±0.01, respectively; the relative expression levels of vascular endothelial growth factor (VEGF) protein were 0.95±0.01, 0.44±0.02, 0.68±0.02 and 0.23±0.01, respectively; the relative expression levels of platelet endothelial cell adhesion molecule-1 (CD31) protein were 1.01±0.01, 0.44±0.02, 0.58±0 and 0.38±0.01, respectively. The above indicators of model group were compared with control group, the above indicators of the oxalic acid group were compared with the model group, and the above indicators of the combination therapy group were compared with the asiatica acid group, the differences were all statistically significant (all P<0.01).

AA can alleviate HCY induced apoptosis of cardiac microvascular endothelial cells and promote vascular regeneration by inhibiting TLR4/MyD88/NF-κB pathway.

To explore the possible mechanisms through which corilagin affects high-glucose-induced oxidative stress and apoptosis in podocytes to alleviate diabetic nephropathy (DN).

MPC5 cells in the logarithmic growth phase were divided into 5 groups: control group (5 mmol·L^-1 glucose), model group (30 mmol·L^-1 glucose), corilagin group (30 mmol·L^-1 glucose plus 50 μM corilagin treatment), corilagin + pcDNA3.1 group (30 mmol·L^-1 glucose plus corilagin 50 μM treatment after transfection with pcDNA3.1), and corilagin + pcDNA3.1-transcription factor 7 (TCF7) group (30 mmol·L^-1 glucose plus corilagin 50 μM treatment after transfection with pcDNA3.1-TCF7). Real-time quantitative polymerase chain reaction (qPCR) was used to detect the expression of long non-coding RNA (LncRNA) TCF7; terminal deoxynucleotidyl transferase dUTP nick-end labeling was employed to assess the apoptosis rate; Western blot was used to analyze the expression of Cleaved caspase-9, Cleaved caspase-3, and proteins related to the glycogen synthase kinase 3 beta (GSK3β)/nuclear factor erythroid-2-related factor2 (Nrf2) signaling pathway; 2′,7′-dichlorofluorescein diacetate fluorescent probe was utilized to measure reactive oxygen species (ROS) levels; and immunofluorescence was used to examine the expression of nephrin and podocin.

The apoptosis rates for the control, model, corilagin, corilagin + pcDNA3.1 and corilagin + pcDNA3.1-TCF7 groups were (5.72±0.49)%, (31.14±5.46)%, (17.01±2.75)%, (16.21±2.83)% and (25.80±3.42)%, respectively; the relative expression levels of Cleaved caspase-9 were 1.00±0.11, 3.91±0.41, 2.43±0.29, 2.49±0.33 and 3.88±0.37, respectively; the relative expression levels for Cleaved caspase-3 were 1.00±0.08, 5.04±0.63, 3.35±0.48, 3.29±0.45 and 4.78±0.56, respectively; the ROS levels were 1.00±0.14, 6.27±1.16, 2.29±0.32, 2.41±0.38 and 5.17±1.08, respectively; malondialdehyde (MDA) levels were (2.33±0.35), (9.26±2.23), (4.80±0.86), (4.47±0.74) and (7.52±1.36) nmol·mg^-1, respectively; superoxide dismutase (SOD) levels were (41.34±6.13), (12.15±1.99), (33.38±4.55), (30.01±4.70) and (24.16±3.71) U·mg^-1, respectively; and catalase (CAT) levels were (68.22±5.45), (28.27±3.48), (52.13±6.06), (50.24±7.43) and (41.91±5.39) U·mg^-1, respectively. When the above indicators in control group compared with those in model group, the above indicators in model group compared with those in the corilagin group, and the above indicators in the corilagin+pcDNA3.1 group compared with those in the corilagin+pcDNA3.1-TCF7 group, all differences showed statistically significant (P<0.05, P<0.01, P<0.001).

Corilagin can inhibit high-glucose-induced oxidative stress and apoptosis in podocytes, thereby alleviating DN, possibly related to its regulation of the GSK3β/Nrf2 signaling pathway by LncRNA TCF7.

To investigate the effects and mechanism of equol on podocyte injury in diabetic nephropathy (DN) by regulating the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway by coiled-coil domain containing 92 (CCDC92).

Mouse MPC5 cells were divided into five groups: the control group (without any treatment), the model group (treated with 30 mmol·L^-1 glucose for 48 h), the experimental group (treated with 1 μmol·L^-1 equol for 24 h on the basis of the model group), the AAV-NC group (transfected with AAV-NC on the basis of the experimental group) and the AAV-CCDC92 group (transfected with AAV-CCDC92 on the basis of the experimental group). Cell viability was detected by the methyl thiazolyl tetrazolium assay. The mRNA level of CCDC92 was determined by real-time fluorescence quantitative polymerase chain reaction. Cell invasive ability was assessed by the transwell assay. The protein relative expression levels of Podocin and Nephrin were detected by immunofluorescence assay. The protein relative expression levels of microtubule-associated protein 1 light chain 3 Ⅱ/Ⅰ (LC3Ⅱ/Ⅰ), Beclin-1, AMPK and mTOR related proteins were measured by Western blot.

The cell viability rates of the control group, model group and experimental group were (100.00±2.84)%, (64.91±9.57)% and (81.36±13.19)%, respectively; the relative expression levels of CCDC92 mRNA in the control group, model group, experimental group, AAV-NC group and AAV-CCDC92 group were 1.00±0.12, 2.26±0.35, 1.42±0.19, 1.48±0.22 and 2.05±0.34, respectively; the number of invasive cells were (79.35±11.62), (25.81±4.06), (53.69±7.95), (60.46±10.58) and (41.13±7.27) cells, respectively; the relative expression levels of Nephrin protein were 1.00±0.14, 0.31±0.05, 0.65±0.09, 0.58±0.08 and 0.39±0.06, respectively; the relative expression levels of Podocin protein were 1.00±0.17, 0.28±0.04, 0.61±0.11, 0.56±0.09 and 0.32±0.06, respectively; the relative expression levels of LC3Ⅱ/Ⅰ protein were 1.00±0.17, 0.26±0.04, 0.74±0.12, 0.69±0.11 and 0.41±0.08, respectively; the relative expression levels of Beclin1 protein were 1.00±0.15, 0.32±0.06, 0.68±0.10, 0.75±0.12 and 0.46±0.07, respectively; the relative expression levels of phosphorylated (p)-AMPK/AMPK protein were 1.00±0.19, 0.23±0.04, 0.86±0.17, 0.89±0.16 and 0.38±0.07, respectively; the relative expression levels of p-mTOR/mTOR protein were 1.00±0.16, 3.16±0.53, 1.72±0.31, 1.65±0.29 and 2.91±0.52, respectively. There were statistically significant differences in the above indicators between the model group and the control group, between the experimental group and the model group and between the AAV-CCDC92 group and the AAV-NC group (P<0.05, P<0.01, P<0.001).

Equol can alleviate podocyte injury in DN through CCDC92, and the effects may be related to regulating the AMPK/mTOR pathway and improving autophagy level.

To investigate the regulatory effects of paeonol on autophagy and the NOD-like receptor protein 3 (NLRP3) inflammasome in human renal proximal tubular epithelial cells (HK-2) induced by human serum albumin (HSA).

HK-2 cells were cultured in vitro and randomly assigned to control group, model group, as well as low-, medium- and high-dose experimental groups. Cells in the control group were cultured under normal conditions; those in the model group were treated with 20 mg·mL^-1 HSA for 24 h; and cells in the low-, medium- and high-dose experimental groups were administered 25, 50 and 100 μmol·L^-1 paeonol, respectively, for 24 h on the basis of the model group intervention. Enzyme-linked immunosorbent assay (ELISA) was performed to determine the concentrations of kidney injury molecule 1 (KIM-1), monocyte chemoattractant protein 1 (MCP-1), interleukin 1β (IL-1β) and caspase-1 in the cell supernatant. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression levels of KIM-1 and MCP-1. Western blotting was applied to measure the protein expression levels of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), interleukin-1β (IL-1β), microtubule-associated protein 1 light chain 3 (LC3), sequestosome 1(p62), Beclin-1, PTEN-induced kinase 1 (PINK1) and Parkin.

The concentrations of KIM-1 in the cell supernatant of the control group, model group, and low-, medium- and high-dose experimental groups were (8.65±0.53), (17.33±2.04), (10.76±1.41), (8.48±0.47) and (8.47±0.24) pg·mL^-1, respectively; the contents of MCP-1 were (531.38±15.64), (2 198.55±148.21), (1 966.29±53.52), (1 605.49±234.68) and (937.33±36.96) pg·mL^-1, respectively; the secretion levels of IL-1β were (71.66±2.29), (109.92±4.41), (91.68±4.75), (80.66±4.00) and (62.38±3.24) pg·mL^-1, respectively; the contents of caspase-1 were (66.57±10.52), (210.50±17.50), (201.88±7.22), (195.42±13.95) and (129.81±13.20) pg·mL^-1, respectively; the relative expression levels of KIM-1 mRNA in each group were 1.05±0.05, 2.38±0.45, 1.58±0.20, 1.44±0.08 and 1.38±0.22, respectively; while those of MCP-1 were 1.04±0.04, 1.53±0.08, 1.32±0.16, 1.16±0.16 and 0.62±0.13, respectively; the relative expression levels of NLRP3 protein were 0.89±0.08, 1.13±0.07, 1.00±0.07, 0.84±0.12 and 0.55±0.16, respectively; those of ASC were 0.23±0.03, 0.87±0.19, 0.81±0.16, 0.78±0.08 and 0.46±0.05, respectively; those of IL-1β were 0.49±0.12, 1.46±0.29, 1.10±0.26, 0.71±0.06 and 0.53±0.13, respectively; the LC3Ⅱ/Ⅰ ratios were 1.08±0.04, 0.90±0.06, 1.00±0.02 and 1.05±0.04, respectively; the expression levels of p62 protein were 0.38±0.06, 1.23±0.11, 1.05±0.20 and 0.62±0.19, respectively; those of Beclin-1 were 0.82±0.07, 0.59±0.06, 0.90±0.07 and 0.93±0.09, respectively; those of PINK1 were 1.10±0.03, 0.68±0.07, 0.78±0.11 and 1.03±0.08, respectively; those of Parkin were 0.64±0.06, 0.46±0.05, 0.58±0.08 and 0.79±0.12, respectively. Compared with the control group, all the above indicators in the model group exhibited statistically significant differences (P<0.05, P<0.01, P<0.001). Moreover, the indicators in the high-dose experimental group showed statistically significant differences compared with the model group (P<0.05, P<0.01, P<0.001).

Paeonol may alleviate albumin-induced renal tubular injury by promoting mitophagy and inhibiting the activation of the NLRP3 inflammasome.

To explore the molecular mechanism by which curcumin (CUR) and chidamide (CHI) synergistically inhibit the malignant behaviors of breast cancer (BC) cells through the interferon (IFN)-retinoic acid-inducible gene Ⅰ (RIG-Ⅰ)-mitochondrial antiviral-signaling protein (MAVS) pathway.

A cellular model was established using MCF-7 breast cancer cells. The cells were divided into five groups: blank group(normol cuttured), CUR group(20 μmol·L^-1 CUR), CHI group(10 μmol·L^-1 CHI), combination group(20 μmol·L^-1 CUR+10 μmol·L^-1 CHI) and inhibitor group(sh-IFN+20 μmol·L^-1 CUR+10 μmol·L^-1 CHI). Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell proliferation capacity was evaluated by plate colony formation assay. Cell migration ability was examined using Transwell and wound healing assays. The relative expression levels of apoptosis-related proteins and IFN-RIG-I-MAVS pathway-associated proteins were detected by Western blotting (WB).

Under CUR concentrations of 0, 10, 20 and 40 μmol·L^-1, the half-maximal inhibitory concentrations (IC₅₀) of CHI were (31.48±2.01), (17.57±0.65), (7.56±0.32) and (0.21±0.02) μmol·L^-1, respectively. Statistically significant dose-dependent reductions in IC₅₀ were observed for CHI when combined with 10, 20 and 40 μmol·L^-1 CUR compared to 0 μmol·L^-1 CUR (all P<0.05). The colony formation numbers were (201.28±23.96) cells for the control group, (113.43±15.59) cells for the CUR group, (109.93±11.64) cells for the CHI group, (59.57±6.91) cells for the combination group, and (87.43±5.04) cells for the inhibitor group, respectively; the numbers of invasive cells were (115.03±13.05), (86.51±9.13), (77.82±6.68), (39.54±5.43) and (68.92±3.95) cells, respectively; the wound closure rates were (51.29±5.17)%, (32.80±2.94)%, (31.23±3.10)%, (16.07±2.11)% and (26.94±1.95)%, respectively; the apoptosis rates were (2.21±0.16)%, (12.03±0.85)%, (12.89±0.99)%, (31.62±2.98)% and (16.85±1.04)%, respectively; the relative expression levels of Caspase-3 were 0.38±0.03, 0.55±0.03, 0.52±0.04, 1.12±0.07 and 0.97±0.05, respectively; the relative expression levels of Caspase-9 levels were 0.33±0.02, 0.53±0.02, 0.55±0.04, 1.05±0.06 and 0.60±0.05, respectively; the relative expression levels of Bax levels were 0.34±0.03, 0.52±0.03, 0.53±0.03, 1.08±0.07 and 0.69±0.06, respectively; the relative expression levels of IFN-β levels were 0.33±0.03, 0.46±0.04, 0.53±0.04, 1.09±0.10 and 0.45±0.03, respectively; the relative expression levels of RIG-Ⅰ levels were 0.32±0.02, 0.57±0.05, 0.65±0.04, 1.02±0.11 and 0.59±0.05, respectively; and the relative expression levels of MAVS levels were 0.34±0.02, 0.41±0.03, 0.49±0.04, 1.04±0.12 and 0.51±0.04, respectively. Statistically significant differences were observed when comparing the CUR and CHI groups to the control group, the combination group to the CUR and CHI groups, and the inhibitor group to the combination group (all P<0.05).

CUR enhances the sensitivity of BC cells to CHI and synergistically exerts anti-BC effects with CHI, and its mechanism of action is related to the activation of the IFN-RIG-I-MAVS pathway by CUR.

To investigate the effects and mechanism of artesunate on hippocampal neuronal damage in schizophrenia rats by adjusting Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.

This study induced a rat model of schizophrenia using ketamine and divided them into model group, low-dose experimental group (5 mg·kg^-1 artesunate), medium-dose experimental group (10 mg·kg^-1 artesunate), and high-dose experimental group (20 mg·kg^-1 artesunate), each with 12 rats. Another 12 rats were considered as normal group. After 21 days of administration, the open field test and three box social behavior experiment were used to detect schizophrenia symptoms in rats; hematoxylin-eosin (HE) staining was used to observe hippocampal neural tissue; Nissl staining was used to observe neuronal damage; terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) staining was used to detect neuronal apoptosis in the hippocampus; enzyme-linked immunosorbent assay (ELISA) was used to detect brain-derived neurotrophic factor (BDNF) in the hippocampus; Western blotting was used to detect JAK1 and STAT3-related protein expression in the hippocampus.

The intersection distances of the central areas of blank group, model group and low, medium and high dose experimental groups were (0.65±0.08), (1.48±0.18), (1.27±0.15), (1.08±0.13) and (0.77±0.09) m, respectively; social interaction times are (63.53±7.39), (31.73±4.09), (38.38±5.32), (44.97±5.13) and (54.78±6.27) s, respectively ; the number of Nissl-positive cells in the hippocampus were (121.38±13.54), (62.63±6.87), (80.85±8.93) , (98.24±9.49) and (118.23±12.63) cells, respectively ; the apoptosis rates were (2.94±0.46)%, (34.73±3.83)%, (25.75±2.92)%, (16.49±2.21)% and (6.83±1.02)%, respectively; the levels of BDNF were (172.58±19.48), (68.49±8.31), (92.26±10.22), (115.08±13.34) and (142.82±16.37) pg·mg^-1, respectively; p-JAK1 protein relative expression levels were 0.38±0.05, 0.87±0.09, 0.73±0.09, 0.60±0.08 and 0.44±0.06, respectively ; p-STAT3 protein relative expression levels were 0.31±0.04, 0.79±0.09, 0.66±0.08, 0.53±0.06 and 0.38±0.05, respectively, when comparing the above indicators between model group and blank group, comparing the above indicators between low, medium, high dose experimental groups and model group, there were statistically significant differences (all P<0.05).

Artesunate may improve hippocampal neuronal damage in schizophrenia rats by inhibiting JAK1/STAT3 signaling pathway.