To investigate the effect of arctigenin on bronchial epithelial cell injury caused by Pseudomonas aeruginosa (PA) infection and its mechanism.

BEAS-2B cells were randomly divided into control group (conventional culture), PA group (1.50×10⁸ CFU·mL^-1 PA infection), PA+ low dose group (PA combined with 10.00 mmol·L^-1 burdock aglycone), PA+ high-dose group (PA combined with 20.00 mmol·L^-1 burdock aglycone). The expression of inflammatory factors and glutathione (GSH) was detected by kit assay, glutathione peroxidase 4 (GPX4) protein was detected by Western blot assay, and lipid peroxidation levels were detected by immunofluorescence assay.

The IL-6 contents of control group, PA group, PA+ low dose group and PA+ high dose group were (20.43±2.82), (106.28±8.07), (76.66±5.73) and (50.57±3.98) pg·mL^-1, respectively; the GSH contents were (25.95±1.46), (10.59±0.60), (13.98±0.74) and (21.52±2.36) ng·mL^-1, respectively; GPX4 protein expression levels were 0.76±0.06, 0.33±0.05, 0.46±0.05 and 0.62±0.06, respectively; the lipid peroxidation levels were (100.00±4.29)%, (470.91±36.33)%, (331.16±27.04)% and (160.16±18.65)%, respectively. The above indexes in PA group compared with control group, PA+ low dose group and PA+ high dose group were compared with PA group, and the differences were all statistically significant (all P<0.01).

Arctigenin can reduce the inflammation of PA-infected BEAS-2B cells by inhibiting GPX4-related ferroptosis pathway.

To observe the clinical efficacy and safety of different doses of atorvastatin calcium tablets combined with trimetazidine hydrochloride tablets in the treatment of patients with chronic heart failure (CHF).

CHF patients were randomly assigned to low-dose group, high-dose group and control group using a digital randomization method. The control group received conventional heart failure treatment in addition to trimetazidine hydrochloride tablets (20 mg per dose, tid). The low-dose group received conventional atorvastatin calcium tablets (20 mg per dose, qd) on basis of the treatment given to the control group. The high-dose group received higher dose of atorvastatin calcium tablets (40 mg per dose, qd) in addition to the treatment for the control group. All treatment continued for 3 months. The clinical efficacy, heart function indicators, three-dimensional myocardial fibrosis parameters, myocardial cell apoptosis-related factors and safety were compared among the three groups.

A total of 8 cases were dropped during the trial, and 30 cases were included in the low-dose group, 24 cases in the high-dose group, and 26 cases in the control group. After treatment, the efficacy rates were 76.67% (23 cases/30 cases) for the low-dose group, 91.67% (22 cases/24 cases) for the high-dose group, and 61.54% (16 cases/26 cases) for the control group. The difference between the high-dose group and the control group was statistically significant (P<0.05). After treatment, the left ventricular ejection fractions for the low-dose group, high-dose group and control group were (52.25±2.11)%, (55.34±2.76)% and (48.72±2.48)%, respectively; the left ventricular end-diastolic diameters were (51.33±3.94), (48.63±4.79) and (55.79±4.85) mm, respectively; the left ventricular end-systolic diameters were (39.77±3.53), (36.72±3.29) and (42.78±3.69) mm, respectively; troponin Ⅰ levels were (1.62±0.33), (1.36±0.29) and (1.84±0.36) ng·L^-1, respectively; N-terminal pro B-type natriuretic peptide levels were (797.25±79.32), (749.20±84.65) and (854.15±90.57) pg·mL^-1, respectively; global strain values were -29.87±5.19, -32.96±5.82 and -26.33±5.46, respectively; cell membrane receptor protein levels were (2.55±0.46), (2.30±0.36) and (2.84±0.50) μg·L^-1, respectively; soluble Fas ligand levels were (0.23±0.06), (0.19±0.04) and (0.28±0.09) μg·L^-1, respectively; the differences among the three groups and between each pair of groups for the above indicators were statistically significant (P<0.05, P<0.01, P<0.001). The main adverse drug reactions in the low-dose group were gastrointestinal bloating and constipation, while the high-dose group primarily experienced constipation. The control group mainly reported nausea. The incidences of adverse drug reactions in the low-dose, high-dose and control groups were 6.67%, 4.17% and 3.85%, respectively, without statistically significant differences (all P>0.05).

The curative effect of intensive dose atorvastain calcium tablets combined with trimetazidine hydrochloride tablets in the treatment of CHF is better than that of conventional dose atorvastatin combined with trimetazidine hydrochloride tablets, and the safety is good.

To observe the clinical efficacy and safety of general anesthesia induction with different doses of remimazolam in the vascular interventional treatment of intracranial aneurysms, and observe the safety.

The patients with intracranial aneurysms who will receive vascular interventional treatment for intracranial aneurysms were divided into low-dose group (0.2 mg·kg^-1 remimazolam), middle-dose group (0.3 mg·kg^-1 remimazolam) and high-dose group (0.4 mg·kg^-1 remimazolam) according to cohoert. The three groups completed intravenous injection of 0.2-0.4 mg·kg^-1 remimazolam. When the consciousness of patients disappeared, 10 μg·kg^-1 alfentanil and 0.2 mg·kg^-1 cisatracurium besilate were used for anesthesia induction, and 0.3-1.0 mg·kg^-1·h^-1 remimazolam+ 0.1 μg·kg^-1·min^-1 remifentanil + 0.2 mg·kg^-1·h^-1 cisatracurium besilate were applied for anesthesia maintenance. The anesthetic effect, heart rate (HR) and mean arterial pressure (MAP) during recovery period, oxidative stress indexes at different time points and, remimazolam remedy were compared among the three groups, and the safety was evaluated.

There were 27 cases in low-dose group, 28 cases in middle-dose group and 25 cases in high-dose group. The HR values at extubation in low-dose group, middle-dose group and high-dose group were (79.47±6.85), (75.84±6.71) and (72.03±5.79) beat·min^-1, HR values at 5 min after extubation were (81.92±6.59), (78.09±7.03) and (74.17±7.26) beat·min^-1, serum superoxide dismutase (SOD) levels at 24 h after surgery were (87.61±11.25), (95.49±14.02) and (103.86±15.37) U·mL^-1, serum malondialdehyde (MDA) levels were (19.69±2.74), (17.24±2.45) and (15.08±2.29) mmol·L^-1, serum catalase (CAT) levels were (66.75±8.39), (71.69±8.55) and (76.91±9.13) U·mL^-1, the onset time of sedation was (94.36±4.42), (82.29±4.15) and (75.17±5.38) s, respectively, and there were significant differences between any two groups of the three groups (all P<0.05). There were 4 cases (14.81%), 0 case and 0 case of remimazolam remedy in low-dose group, middle-dose group and high-dose group, respectively, and the index in middle-dose group and high-dose group was significantly different compared with that in low-dose group (P<0.05). In the low-dose group, there was 1 case (3.70%) of hypotension, 1 case (3.70%) of respiratory depression, and 2 cases (7.41%) of intraoperative body movement. In the middle-dose group, there was 1 case (3.70%) of hypotension, 1 case (3.57%) of bradycardia, and 1 case (3.70%) of respiratory depression. In the high-dose group, there was 1 case (4.00%) of hypotension, 2 cases (8.00%) of bradycardia, and 2 cases (8.00%) of respiratory depression. There was no statistically significant difference in the incidence of adverse drug reactions among the three groups (all P>0.05).

The induction of general anesthesia with different doses of remimazolam has a certain application effect in the vascular interventional treatment of intracranial aneurysms, and the induction of general anesthesia with high doses of remimazolam (0.4 mg·kg^-1) is the most ideal. It is not only beneficial to maintaining the stability of hemodynamics during the recovery period, and alleviating the oxidative stress response, but also shortening the onset time of sedation, reduce the number of remedial cases, and it has good safety.

To investigate the effect of anemoside B4 on the malignant biological behavior of non-small cell lung cancer (NSCLC) cells mediated by microRNA-142-3p (miR-142-3p) on the expression of high mobility group protein A1 (HMGA1).

A549 cells were divided into A549 group (normal culture), anemoside B4 group (100 μg·mL^-1 anemoside B4 treatment), inhibitor NC group (100 μg·mL^-1 anemoside B4+ transfection inhibitor NC treatment), miR-142-3p inhibitor group (100 μg·mL^-1 anemoside B4+ transfected with miR-142-3p inhibitor treatment), si-NC group (100 μg·mL^-1 anemoside B4+ co-transfected with miR-142-3p inhibitor and si-NC treatment), si-HMGA1 group (100 μg·mL^-1 anemoside B4+ co-transfected with miR-142-3p inhibitor and si-HMGA1 treatment). Real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting (WB) were used to detect the expression of miR-142-3p and HMGA1. Cell proliferation, migration and apoptosis were detected by 5-acetylidene-2′-deoxyuracil riboside (Edu), Transwell and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL).

The miR-142-3p relative expression levels of A549 group, anemoside B4 group, inhibitor NC group and miR-142-3p inhibitor group were 1.00±0.14, 1.58±0.18, 1.60±0.21 and 1.12±0.16, respectively; the relative expression levels of HMGA1 protein were 1.00±0.23, 0.56±0.07, 0.59±0.08 and 0.95±0.21, respectively; the proliferation rates were (84.62±9.11)%, (62.15±7.20)%, (63.89±7.77)% and (76.35±8.11)%, respectively; the migration number was (156.23±17.54), (80.65±8.67), (82.15±8.96) and (111.55±12.75) cells, respectively; the apoptosis rates were (8.96±0.95)%, (32.56±3.56)%, (33.95±3.79)% and (16.89±1.92)%, respectively. The proliferation rates of si-NC group and si-HMGA1 group were (75.98±8.05)% and (64.52±7.25)%, respectively; the migration number was (118.85±12.98) and (86.95±9.21) cells, and the apoptosis rates were (17.58±2.02)% and (28.15±3.13)%, respectively. The above indexes in A549 group were compared with anemoside B4 group, miR-142-3p inhibitor group were compared with inhibitor NC group, si-HMGA1 group were compared with si-NC group, the differences were all with statistically significant (all P<0.05).

Anemoside B4 may inhibit proliferation and migration of NSCLC cells and promote apoptosis by regulating the miR-142-3p/HMGA1 axis.

To observe the clinical efficacy and safety of evolocumab injection combined with pitavastatin calcium tablets in the treatment of patients with acute coronary syndrome after percutaneous coronary intervention (PCI).

According to cohort method, the patients with acute coronary syndrome after PCI were divided into control group and treatment group. Two groups were treated with routine treatment (anti-platelet, anti-coagulation, reducing myocardial oxygen consumption, improving myocardial ischemia). On the routine treatment, control group was treated with pitavastatin calcium 2 mg per time, once a day, orally before bedtime. On the basis of control group, treatment group was given evolocumab 140 mg per time, once every 2 weeks, subcutaneous injection. Two groups were treated for 6 months. The clinical efficay, blood lipid, myocardial injury indexes, serum levels of amyloid A1 (SAA1) and Gla-rich protein (GRP), major adverse cardiovascular events (MACEs) and safety were compared between two groups.

Fifty-two patients were enrolled in the treatment group and 58 patients were enrolled in the control group. After treatment, the total effective rates of treatment and control groups were 94.23% (49 cases/52 cases) and 75.86% (44 cases/58 cases), and the difference was statistically significant (P<0.05). After treatment, the total cholesterol levels of treatment and control groups were (1.17±0.22) and (1.35±0.25) mmol·L^-1, triglyceride levels were (2.63±0.76) and (3.89±0.92) mmol·L^-1, high-density lipoprotein cholesterol levels were (1.41±0.30) and (1.26±0.28) mmol·L^-1, low-density lipoprotein cholesterol levels were (1.23±0.46) and (1.58±0.55) mmol·L^-1, cardiac troponin I levels were (0.03±0.01) and (0.05±0.02) ng·mL^-1, creatine kinase isoenzyme levels were (12.35±2.38) and (14.23±2.89) U·L^-1, SAA1 levels were (213.92±41.58) and (274.18±43.36) μg·mL^-1, GRP levels were (21.32±3.50) and (19.35±3.27) ng·mL^-1, incidences of MACEs were 9.62% and 24.14%, the differences were statistically significant between two groups (all P<0.05). The adverse drug reactions of two groups were fatigue, pruritus, abdominal pain and elevated aminotransferase. There was no significant difference in total incidences of adverse drug reactions between treatment group and control group (11.54% vs 13.79%, P>0.05).

Evolocumab injection combined with pitavastatin calcium tablets has a definitive clinical efficacy in the treatment of patients with acute coronary syndrome after PCI, which can effectively reduce the blood lipid levels, the incidence of MACEs and myocardial injury, regulate the serum levels of SAA1 and GRP, without increasing the incidence of adverse drug reactions.

To observe the effect and safety of dydrogesterone combined with estradiol valerate on preventing the intrauterine re-adhesion after intrauterine adhesion (IUA) surgery.

The patients after IUA surgery were divided into control group and treatment group according to the cohort method. The control group was given oral estradiol valerate tablets (2 mg every time, twice a day) immediately after surgery and stopped after 30 days of continuous oral administration, and on the basis of the control group; the treatment group received dydrogesterone tablets (10 mg each time, once a day) from the 20^th day until the next menstruation. Both groups were treated for 2 menstrual cycles. The efficacy, endometrial receptivity ultrasound parameters [endometrial thickness, endometrial volume, vascular index (VI), blood flow index (FI), vascular blood flow index (VFI)], sex hormones [estradiol (E2), follicle stimulating hormone (FSH), luteinizing hormone (LH)], adverse reactions and occurrence of re-adhesion were compared between the two groups.

Forty-eight cases in treatment group and 44 cases in control group were finally included. After 2 menstrual cycles of treatment, the total effective rates in treatment group and control group were 95.83% (46 cases/48 cases) and 81.82% (36 cases/44 cases), respectively (P<0.05). After 2 menstrual cycles of treatment, the endometrial thicknesses in treatment group and control group were (7.88±1.02) and (7.12±0.86) mm; the endometrial volumes were (3.02±0.97) and (2.57±0.73) cm³; VI values were 1.21±0.59 and 0.88±0.57; FI values were 29.87±5.12 and 27.56±4.63; VFI values were 1.12±0.43 and 0.83±0.36; E2 levels were (239.62±25.47) and (168.91±20.12) pmol·L^-1; FSH levels were (8.94±2.02) and (10.63±2.14) U·L^-1; LH levels were (13.38±2.16) and (15.27±2.59) U·L^-1, respectively (all P<0.05). The adverse drug reactions in treatment group were mainly breast tenderness and digestive tract discomfort; and the adverse drug reactions in control group were mainly breast tenderness, digestive tract discomfort and headache. The total incidence rates of adverse drug reactions in treatment group and control group were 14.58% (7 cases/48 cases) and 11.36% (5 cases/44 cases), respectively (P>0.05). The incidence rates of re-adhesion in treatment group and control group were 6.25% (3 cases/48 cases) and 20.45% (9 cases/44 cases) (P<0.05).

Dydrogesterone combined with estradiol valerate has a significant effect on preventing intrauterine re-adhesion after IUA surgery, and it can effectively improve the endometrial receptivity and sex hormones levels of patients, and it has medication safety.

To investigate the effect and mechanism of ursodeoxycholic acid on bronchial epithelial cell injury induced by toluene diisocyanate (TDI).

BEAS-2B cells were randomly divided into control group (conventional culture), TDI-human serum albumin (HSA) group (120.00 mg·L^-1 TDI-HSA), low-dose group (100 μmol·L^-1 ursodeoxycholic acid+120.00 mg·L^-1 TDI-HSA), high-dose group (200 μmol·L^-1 ursodeoxycholic acid+120.00 mg·L^-1 TDI-HSA) and rapamycin group (25 nmol·L^-1 rapamycin+120.00 mg·L^-1 TDI-HSA). The expression of inflammatory factors was detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA); the level of reactive oxygen species (ROS) was detected by DCFH-DA; and the protein expression of each cell was detected by Western blot.

The mRNA levels of interleukin (IL)-6 in control group, TDI-HSA group, low-dose group and high-dose group were 1.00±0.13, 2.20±0.24, 1.87±0.12, 1.48±0.14, respectively; IL-8 levels were (22.65±1.96), (81.42±6.35), (56.36±5.88), (38.28±3.25) pg·mL^-1, respectively; ROS levels were (100.00±3.47)%, (351.25±22.52)%, (312.80±26.59)%, (242.15±13.60)%, respectively; the protein levels of dynamic associated protein 1 (DRP1) were 0.23±0.03, 0.82±0.08, 0.69±0.10, 0.55±0.05, respectively; benzyl chloride 1 (Beclin1) protein expression levels were 0.23±0.04, 0.60±0.07, 0.44±0.04, 0.37±0.03, respectively; phosphorylated adenylate activates protein kinase (p-AMPK) protein expression levels were 0.20±0.05, 0.49±0.05, 0.40±0.03, 0.34±0.04, respectively. Beclin1 protein expression levels in high-dose group and rapamycin group were 0.35±0.04 and 0.69±0.07, respectively; IL-6 levels were (17.63±1.36) and (29.52±3.49) pg·mL^-1, respectively; IL-18 levels were (65.22±5.30) and (95.58±6.80) pg·mL^-1, respectively. The above indexes: TDI-HSA group was compared with control group, low- dose group and high- dose group were compared with TDI-HSA group, rapamycin group compared with high dose group, the differences were significant (all P<0.05).

Ursodeoxycholic acid may mediate ROS/AMPK/ autophagy pathway to improve the inflammatory response and mitochondrial dysfunction induced by TDI-HSA.

To observe the anesthetic effects and safety of remazolam injection combined with alfentanil injection in the treatment of patients with hysteroscopic surgery.

Patients scheduled for hysteroscopic surgery were randomly divided into control group and treatment group. The control group received intravenous 1.5-2.0 mg·kg^-1 propofol + 7-10 μg·kg^-1 alfentanil for anesthetic induction, during the surgery, continuously infused with 4-12 mg·kg^-1·h^-1 propofol + 0.05-0.20 μg·kg^-1·h^-1 remifentanil for anesthesia maintenance. The treatment group was given intravenous 0.3-0.5 mg·kg^-1 remimazolam + 7-10 μg·kg^-1 alfentanil for anesthetic induction, during the surgery, received 0.5-1.0 mg·kg^-1·h^-1remazolam+ 0.05-0.20 μg·kg^-1·h^-1 remifentanil for anesthesia maintenance. The hemodynamics, analgesic effects, cognitive function and safety were compared between the two groups.

Control group were enrolled 52 cases, 3 cases dropped out, and 49 cases were finally included in the statistical analysis. Treatment group were enrolled 53 cases, 4 cases dropped out, and 49 cases were finally included in the statistical analysis. At the end of the surgery, the mean arterial pressure of treatment and control groups were (73.98±7.41) and (60.10±6.84) mmHg, the heart rates were (68.43±7.32) and (63.92±7.36) beat·min^-1, the differences of above index were statistically significant between two groups (all P<0.05). One hour after operation, the visual analogue scale scores of treatment and control groups were (3.08±0.49) and (3.86±0.61) points, the mini-mental state examination scores were (22.65±2.41) and (18.24±2.38) points, the differences were statistically significant (all P<0.05). The adverse drug reactions of treatment group were nausea, while those in the control group were bradycardia, hypotension, respiratory depression and nausea. The total incidences of adverse drug reactions in the treatment and control groups were 2.04% and 14.29%, with statistically significant difference (P<0.05).

Remazolam injection combined with alfentanil injection can help to maintain hemodynamics of patients with hysteroscopic surgery, reduce the risk of postoperative pain and cognitive impairment, with good safety.

To observe the clinical effect and safety of N-acetylcysteine combined with budesonide and terbutaline in the treatment of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and respiratory failure (RF).

According to queuing method, patients with AECOPD and RF were divided into treatment group and control group. On basis of basic treatment, control group was given aerosol inhalation of budesonide suspension (1 mg/once, bid) and terbutaline solution (5 mg/once, bid), while treatment group was given aerosol inhalation of N-acetylcysteine solution (0.3 g/once, bid) on basis of control group. All patients were treated for 2 weeks. The clinical effect, pulmonary function indexes [forced vital capacity (FVC), peak expiratory flow (PEF)], dyspnea degree [modified version of British medical research council dyspnea scale (mMRC)], oxidative stress response indexes [superoxide dismutase (SOD)] and inflammatory response indexes [hypersensitive C-reactive protein (hs-CRP)] were compared between the two groups after treatment, and safety was evaluated.

There were 56 cases in control group and 64 cases in treatment group. After treatment, the total effective rate of the treatment group and the control group were 93.75% (60 cases /64 cases) and 82.14% (46 cases /56 cases), respectively, and the difference was statistically significant (P<0.05). After treatment, FVC in treatment group and control group were (2.41±0.59) and (2.08±0.54) L; PEF were (4.97±1.18) and (4.08±1.12) L·s^-1; mMRC scores were (1.86±0.39) and (2.67±0.56) points; SOD levels were (97.54±8.03) and (79.02±7.27) U·L^-1; hs-CRP levels were (5.09±1.42) and (8.63±2.13) mg·L^-1. Compared with control group, the above indexes in treatment group were statistically significant (all P<0.001). The adverse drug reactions in treatment group were mainly on vomiting, rash, palpitation and nausea, while in control group were mainly on fatigue, gastrointestinal reactions and rash. There was no significant difference in total incidence of adverse drug reactions between treatment group and control group [10.94% (7 cases/64 cases) vs 8.93% (5 cases/56 cases), P>0.05].

Curative effect of N-acetylcysteine combined with budesonide and terbutaline is significant in patients with AECOPD and RF, which can promote the recovery of pulmonary function, relieve dyspnea, oxidative stress and inflammatory response.

To investigate the cardioprotective mechanism of Ilexin A in ameliorating hyperlipidemia through the regulation of microRNA-133a-3p (miR-133a-3p) and uncoupling protein 2 (UCP2).

Rats were randomly divided into control group (gavage with an equal volume of distilled water as the experimental group), model group (gavage with an equal volume of distilled water as the experimental group), experimental group (gavage with 40 mg·kg^-1 Ilexin A), miR-133a-3p inhibitor group (gavage with 40 mg·kg^-1 Ilexin A + tail vein injection of 1.95×10¹² vg·mL^-1 adenovirus containing miR-133a-3p inhibitor), and OE-UCP2 group (gavage with 40 mg·kg^-1 Ilexin A + tail vein injection of 1.95×10¹² vg·mL^-1 adenovirus containing both miR-133a-3p inhibitor and OE-UCP2). Blood lipid levels, including low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C), were measured by enzyme-linked immunosorbent assay. Cardiac function parameters, such as the mitral inflow peak early diastolic velocity to late diastolic velocities (E/A) and left ventricular ejection fraction (LVEF), were assessed via echocardiography. The relative expression levels of mRNA were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR), while protein levels were detected by Western blot.

In the model and experimental groups, LDL-C levels were (0.92±0.12) and (0.76±0.09) mmol·L^-1; HDL-C levels were (0.82±0.10) and (1.14±0.13) mmol·L^-1; E/A ratios were 0.89±0.11 and 1.17±0.14; LVEF values were (41.31±5.07)% and (59.92±7.86)%; the relative expression levels of miR-133a-3p were 0.33±0.06 and 1.22±0.18; uncoupling protein 2 (UCP2) mRNA levels were 0.57±0.08 and 0.79±0.09; cleaved caspase-3 protein levels were 1.00±0.15 and 0.71±0.09; B-cell lymphoma-2 (Bcl-2) protein levels were 1.00±0.17 and 1.94±0.27, respectively. The differences between the model and experimental groups for these parameters were statistically significant (all P<0.05).

Ilexin A ameliorates hyperlipidemia by regulating miR-133a-3p and UCP2. Its mechanism may involve downregulating Bcl-2 and activating cleaved caspase-3 to induce apoptosis, thereby exerting cardioprotective effects and improving cardiac function.