To observe the efficacy and safety of bifidobacterium triple viable capsule in patients with type Ⅲ prostatitis.

Patients with type Ⅲ prostatitis in the hospital were retrospectively selected and divided into treatment group and control group. The two groups of patients both took sertraline tablets 0.05 g, once daily. Patients in control group were given oral administration of 0.2 mg of tamsulosin sustained release capsule once a day, while patients in treatment group received oral administration of 0.42 g of bifidobacterium triple viable capsule twice a day on the basis of control group. Both groups were treated for 4 weeks. The efficacy, clinical symptoms scores, urodynamic parameters and inflammatory factors were compared between the two groups, and the safety was evaluated.

A total of 200 patients were enrolled, including 97 cases in control group and 103 cases in treatment group. After 4 weeks of treatment, the total effective rate in treatment group was 88.35% (91 cases/103 cases), which was statistical significant higher than 79.38% (77cases/97 cases) in control group (P>0.05). After treatment, the scores of the pain domain of the national institutes of health chronic prostatitis symptom index (NIH-CPSI) in treatment group and control group were (4.37±1.42) and (5.04±1.56) point, respectively; the self-rating depression scale (SDS) scores were (38.20±5.38) and (40.63±5.54) point, respectively; the levels of interleukin-6 (IL-6) were (5.93±1.08) and (6.30±1.27) pg·mL^-1, respectively; the levels of interleukin-10 (IL-10) were (6.21±1.37) and (6.62±1.49) pg·mL^-1, respectively; and the levels of cyclooxygenase-2 (COX-2) were (9.46±2.66) and (10.26±2.02) ng·mL^-1, respectively. There were statistical significant differences in the above indicators between treatment and control group (all P<0.05). The main adverse drug reactions in treatment group included dizziness, nausea and vomiting, and diarrhea, whereas dizziness and diarrhea occurred in control group. The overall incidence of adverse drug reactions was 4.85% (5 cases/103 cases) in treatment group and 2.06% (2 cases/97 cases) in control group, with no statistically significant difference between the two groups (P>0.05).

Bifidobacterium triple viable capsule in the treatment of type Ⅲ prostatitis can improve the pain symptom and depression, and regulate the levels of inflammatory factors, and it has good safety.

To observe the clinical efficacy and safety of the application of bromhexine hydrochloride injection combined with high-flow nasal cannula oxygen therapy in children with severe pneumonia complicated with type I respiratory failure.

Children with severe pneumonia complicated with type I respiratory failure who were treated in our hospital were collected and divided into control group and treatment group based on the treatment methods. The control group received conventional oxygen therapy on the basis of conventional treatment, while the treatment group was given bromhexine hydrochloride and glucose injection (2~4 mg each time, qd, intravenous drip) combined with high-flow nasal cannula oxygen therapy on the basis of conventional treatment. Both groups were treated for 7 days. The clinical efficacy, respiratory and circulatory indicators, and inflammatory indicators of the two groups were compared, and safety was evaluated.

A total of 94 children were included, including 49 in control group and 45 in treatment group. After treatment, the overall clinical response rates were 75.51% (37 cases/49 cases) in control group and 91.11% (41 cases /45 cases) in treatment group, demonstrating a statistically significant difference (P<0.05). After treatment, the arterial partial pressure of oxygen (PaO₂) levels of control group and treatment group were (75.43±7.71) and (80.35±8.63) mmHg, respectively; the percutaneous oxygen saturation (SpO₂) levels were (94.16±2.06)% and (95.31±2.33)%, respectively; the PaO₂/FiO₂ levels were 327.08±34.36 and 342.40±33.53, respectively; the respiratory rate (RR) levels were (30.16±3.39) and (28.33±3.03) time·min^-1, respectively; the lactate levels were (2.66±0.43) and (2.38±0.34) mmol·L^-1, respectively; the interleukin-6 (IL-6) levels were (14.45±3.37) and (12.64±3.31) pg·mL^-1, respectively; the white blood cell (WBC) levels were (7.94±2.13) and (7.07±1.87) ×10⁹·L^-1, respectively; the neutrophil percentage (NEUT%) levels were (55.36±8.25)% and (51.58±7.43)%, respectively; the procalcitonin (PCT) levels were (0.17±0.04) and (0.15±0.04) ng·mL^-1, respectively, all differences between the two groups were statistically significant (P<0.05, P<0.01). The main adverse drug reactions in control group were facial skin damage, nasal mucosa damage and abdominal distension; the main adverse drug reactions in treatment group were nausea, vomiting, facial skin damage and nasal mucosa damage. The total incidence of adverse drug reactions in control group and treatment group were 14.29% (7 cases/49 cases) and 11.11% (5 cases/45 cases), respectively, with no statistically significant difference (P>0.05).

The treatment plan of bromhexine hydrochloride and glucose injection combined with high-flow nasal cannula oxygen therapy for children with severe pneumonia complicated with type Ⅰ respiratory failure is effective. It can significantly improve clinical symptoms, shorten the time of symptom relief, improve respiratory and circulatory indicators, reduce inflammatory indicators, promote the absorption of pneumonia, improve treatment comfort, shorten hospital stay and has good safety.

To observe the clinical efficacy and safety of programmed death-1 (PD-1) inhibitors (tislelizumab injection or sintilimab injection) combined with the capecitabine tablet and oxaliplatin for injection regimen (XELOX) as first-line treatment in patients with advanced gastric signet-ring cell carcinoma (SRCC)

Patients with SRCC were enrolled and divided into control group and treatment group using a random number table. The control group received the XELOX regimen, 130 mg·m^-2 intravenous oxaliplatin for injection on day 1, and oral 1 000 mg·m^-2 capecitabine tablets twice daily from days 1 to 14, repeated every 21 days. The treatment group received an intravenous infusion of tislelizumab injection or sintilimab injection 200 mg per dose prior to the XELOX regimen, also administered every 21 days. Both groups were treated for 6 cycles. Clinical efficacy, tumor markers, immune function, clinical scores, safety and long-term prognosis were compared between the two groups.

A total of 82 patients were included, with 41 cases in each group. The levels of carcinoembryonic antigen (CEA) in treatment and control group were (6.46±1.03) and (7.00±0.94) ng·mL^-1, respectively; the levels of carbohydrate antigen 19-9 (CA19-9) were (18.62±3.36) and (20.58±3.52) U·mL^-1, respectively; vascular endothelial growth factor (VEGF) were (33.57±5.56) and (36.15±5.03) ng·mL^-1, respectively; CD3⁺ T cells were (62.31±5.71)% and (59.50±6.10)%, respectively; CD4⁺ T cells were (47.56±5.93)% and (44.91±4.84)%, respectively; European organisation for research and treatment of cancer quality of life questionnaire core 30 (QLQ-C30) score were (60.15±11.01) and (55.02±9.46) points, respectively; and revised piper fatigue scale (RPFS) score were (5.05±0.89) and (5.49±0.84) points, respectively; the levels of CA72-4 were (34.07±3.74) and (36.23±3.01) U·mL^-1, respectively; the CD4⁺/CD8⁺ ratios were 1.99±0.35 and 1.75±0.37, respectively; the differences of above indicators between two groups were all statistically significant (P<0.05, P<0.01). Adverse drug reactions in both groups were gradeⅠorⅡand resolved after drug discontinuation. The incidence of adrenal dysfunction in the treatment group was 14.63% (6 cases/41 cases), which was significantly higher than that in the control group (0%) (P<0.05). The median survival time was 38 months in the treatment group and 28 months in the control group (P<0.05).

PD-1 inhibitors (tislelizumab or sintilimab injection) combined with the XELOX regimen as first-line therapy can enhance the efficacy in patients with advanced SRCC, significantly improve quality of life and long-term survival benefits, and exhibit a favorable safety profile. This therapeutic advantage may be attributed to the regimen’s effect on downregulating tumor markers and improving immune function.

To explore the potential mechanism of cinnamaldehyde in alleviating nerve injury in rats with traumatic brain injury (TBI).

Rats were randomly divided into sham group (only craniotomy), model group(TBI model), experimental-L group (TBI+25 mg·kg^-1 cinnamaldehyde), experimental-H group (TBI+75 mg·kg^-1 cinnamaldehyde), miR-NC group (TBI+miR-NC lentivirus+75 mg·kg^-1 cinnamaldehyde) and miR-27a-3p inhibitor group (TBI+miR-27a-3p inhibitor lentivirus+75 mg·kg^-1 cinnamaldehyde). After treatment, real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-27a-3p; the Morris water maze test was used to assess memory function; immunofluorescence assay was used to detect the expression of ionized calcium-binding adapter molecule 1 (Iba-1); Western blot was used to detect the expression of related proteins in brain tissues; and the dual-luciferase reporter gene assay was used to verify the binding of miR-27a-3p to BCL2/adenovirus E1B 19kDa interacting protein 3-like (BNIP3L).

The relative expression levels of miR-27a-3p in the sham group, model group, experimental-L group, experimental-H group, miR-NC group and miR-27a-3p inhibitor group were 1.00±0.08, 0.40±0.03, 0.52±0.08, 0.76±0.08, 0.73±0.09 and 0.18±0.02, respectively; the escape latency times were (11.19±0.75), (26.06±1.47), (23.59±1.39), (14.95±1.71), (15.37±0.77) and (24.91±1.96) s, respectively; the Iba-1 fluorescence intensities were (1 189.50±113.68), (2 958.70±279.29), (2 287.05±271.69), (1 916.55±205.44), (1 935.57±164.54) and (2 564.52±333.05) a.u., respectively; the relative expression levels of autophagy-related gene 5 (ATG5) protein were 0.32±0.03, 0.94±0.07, 0.71±0.09, 0.50±0.08, 0.53±0.07 and 0.85±0.09, respectively; the relative expression levels of Beclin-1 autophagy regulator (Beclin-1) protein were 0.35±0.03, 0.95±0.13, 0.75±0.12, 0.49±0.05, 0.48±0.07 and 0.73±0.10, respectively; the relative expression levels of Parkin RBR domain E3 ubiquitin protein ligase (Parkin) protein were 0.29±0.04, 0.64±0.08, 0.51±0.09, 0.41±0.04, 0.43±0.05 and 0.62±0.07, respectively. For the above indicators, there were all statistically significant differences when comparing the model group with the sham group, the experimental-L and experimental-H groups with the model group, and the miR-27a-3p inhibitor group with the miR-NC group (P<0.05, P<0.01, P<0.001). The dual-luciferase reporter gene assay confirmed the targeted binding of miR-27a-3p to BNIP3L.

Cinnamaldehyde may regulate autophagy through the miR-27a-3p/BNIP3L axis, improve neurological function, alleviate neuroinflammation and exert neuroprotective effects on TBI-induced brain injury.

To investigate the ameliorative effects of curculigoside on rats with aortic dissection by the inhibition of the reactive oxygen species /NOD-like receptor thermal protein domain associated protein 3 (ROS/NLRP3) pathway.

Rats were randomly divided into control group, model group, low-dose experimental group (50 mg·kg^-1 curculigoside), high-dose experimental group (100 mg·kg^-1 curculigoside) and combination group (100 mg·kg^-1 curculigoside and 1.75 mg·mL^-1 trimethylamine N-oxide), with 12 rats in each group. The rat model of aortic dissection was established by intragastric administration of 0.1 g·kg^-1 β-aminopropionitrile (BAPN). Cardiac blood was collected, and the levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay (ELISA). hematoxylin-eosin (HE) staining and Van Gieson staining were used to evaluate histopathological changes and the degree of elastic fiber rupture. Reactive oxygen species (ROS) levels were detected using 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining. The mRNA expression levels of matrix metalloproteinase 9 (MMP-9) and matrix metalloproteinase 2 (MMP-2) in aortic tissues were measured by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). The protein expression levels of apoptosis-associated speck-like protein containing a CARD (ASC), NLR family pyrin domain-containing 3 (NLRP3) and caspase-1 in aortic tissues were detected by Western blotting.

The IL-6 levels in the low-dose experimental group, high-dose experimental group, control group, model group and combination group were (49.06±4.98), (37.18±3.81), (35.62±3.63), (72.34±7.33) and (50.03±5.08) pg·mL^-1, respectively; the TNF-α levels were (25.63±2.64), (16.35±1.71), (15.31±1.62), (42.06±4.23) and (26.15±2.64) pg·mL^-1, respectively; the degrees of elastic fiber rupture were 2.01±0.22, 0.85±0.09, 0±0, 3.22±0.34 and 1.85±0.19, respectively; the ROS levels were 358.62±36.64, 203.11±20.15, 186.34±19.11, 588.64±60.03 and 361.24±37.24, respectively; the relative mRNA expression levels of MMP-9 were 1.67±0.18, 1.15±0.12, 1.02±0.11, 2.45±0.26 and 1.72±0.19, respectively; the relative mRNA expression levels of MMP-2 were 1.88±0.19, 1.24±0.14, 0.98±0.10, 2.85±0.30 and 1.91±0.20, respectively; the relative protein expression levels of Caspase-1 were 0.85±0.09, 0.55±0.06, 0.44±0.05, 1.24±0.13 and 0.88±0.10, respectively; the relative protein expression levels of ASC were 0.97±0.10, 0.64±0.08, 0.55±0.06, 1.48±0.16 and 0.89±0.09, respectively; and the relative protein expression levels of NLRP3 were 0.64±0.08, 0.35±0.05, 0.25±0.03, 1.02±0.11 and 0.72±0.09, respectively. Compared with the control group, the above indicators in the model group were significantly different (all P<0.05); compared with the model group, the above indicators in the high-dose experimental group were significantly different (all P<0.05); and compared with the high-dose experimental group, the above indicators in the combination group were significantly different (all P<0.05).

Curculigoside can effectively ameliorate BAPN-induced aortic injury in rats. Its protective mechanism against the development of aortic dissection may be associated with the inhibition of the ROS/NLRP3 signaling pathway.

To investigate the effects of celastrol (Cel) on airway remodeling factors, collagen synthesis and degradation in lung fibroblasts of chronic obstructive pulmonary disease (COPD) rats by regulating the neurogenic locus notch homolog protein (Notch) pathway.

A total of 30 rats were randomly divided into 3 groups: animal control group (normal feeding), animal model group (COPD rat model established by smoke exposure combined with lipopolysaccharide tracheal instillation) and animal experimental group (intraperitoneal injection of 0.01 mg·kg^-1 Cel after successful modeling). The bronchial fibroblasts (BF) cells were isolated from rats in the animal model group and randomly divided into cell control group (no treatment), cell experimental group (2 μmol·L^-1 Cel) and inhibitor group [1 mmol·L^-1 valproic acid (VPA)]. Pulmonary function was assessed in rats using invasive pulmonary function testing methods; Western blot was used to detect the expression of Notch signaling pathway-related proteins in each group of cells; real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect mRNA expression of airway remodeling-related factors; enzyme-linked immunosorbent assay (ELISA) was used to detect the contents of matrixmetalloproteinase-1 (MMP-1) and tissue inhibitors of metalloproteinase-1 (TIMP-1) in each group of cells.

The forced vital capacity (FVC) of rats in animal control group, animal model group and animal experimental group were (6.74±0.87), (3.28±0.51) and (4.94±0.83) mL, respectively; the forced expiratory volume in 0.1 second (FEV0.1) were (3.94±0.45), (1.05±0.16) and (2.41±0.37) mL, respectively; the peak expiratory flow (PEF) were (28.09±4.60), (16.63±3.21) and (21.55±4.02) L·min^-1, respectively. Significant differences were observed in the above indicators between animal control group and animal model group, and between animal model group and animal experimental group (P<0.01, P<0.001). The relative expression levels of (Notch1) protein in cell control group, cell experimental group and inhibitor group were 1.00±0.19, 0.12±0.02 and 0.38±0.06, respectively; the relative expression levels of Notch1 receptor intracellular binding domain (NICD1) protein were 1.00±0.17, 0.72±0.12 and 0.85±0.13, respectively; the relative expression levels of serrated typical Notch ligand 1 (Jagged1) protein were 1.00±0.15, 0.71±0.11 and 0.84±0.12, respectively; the relative expression levels of hair and enhancer of split 1 (Hes1) protein were 1.00±0.11, 0.69±0.08 and 0.81±0.09, respectively; the relative expression levels of MMP-9 mRNA were 1.00±0.16, 0.59±0.08 and 0.73±0.11, respectively; the relative expression levels of type Ⅰ collagen(ColⅠ) mRNA were 1.00±0.14, 0.67±0.09 and 0.86±0.14, respectively; the relative expression levels of α-smoth muscle actin (α-SMA) mRNA were 1.00±0.16, 0.41±0.07 and 0.78±0.13, respectively; the relative expression levels of transforming growth factor-β (TGF-β) mRNA were 1.00±0.18, 0.53±0.09 and 0.75±0.14, respectively; the contents of MMP-1 were (1.19±0.17), (0.80±0.15) and (1.06±0.15) ng·mL^-1, respectively; the contents of tissue inhibitor of protease-1 (TIMP-1) were (219.78±30.24), (131.94±18.15) and (167.51±21.01) ng·mL^-1, respectively. There were all statistically significant differences in the above indicators between cell control group and cell experimental group, as well as between cell experimental group and inhibitor group (P<0.05, P<0.01, P<0.001).

Celastrol can effectively improve lung function and pulmonary pathological damage in COPD rats, reduce the levels of inflammatory cells and inflammatory factors, and improve the imbalance of airway remodeling-related factors and collagen synthesis/degradation in BF cells, which may be related to its inhibition of Notch signaling activation.

To investigate the effects and mechanism of nobiletin (NOB) on slow transit constipation (STC) in rats through dopamine receptor D2 (DRD2).

A total of 70 SD rats were randomly divided into blank group, model group, experimental-L, M, H group, AAV9-NC group and AAV9-DRD2 group, with 10 rats in each group. STC model was established with 15 mg·kg^-1 compound diphenoxylate by intragastric administration except in blank group. In experimental-L, M, H group, 0.1, 0.2, 0.4 g·kg^-1 NOB was administered intragastricly. On the basis of experimental-M group, AAV9-NC group and AAV9-DRD2 group were given AAV9-NC and AAV9-DRD2 100 μL, respectively. Weight and fecal indexes of rats were detected. The expression levels of DRD2 was detected by quantitative real time polymerase chain reaction. Vasoactive intestinal peptide (VIP) and nitric oxide (NO) levels were detected by enzyme-linked immunosorbent assay. Levels of AMP-activated protein kinase (AMPK)/endothelial nitric oxide synthase (eNOS) signaling pathway related proteins were detected by Western blot.

The fecal water content in blank, model, and experimental-L, M, H groups were (35.24±5.25)%, (24.76±3.47)%, (28.38±2.77)%, (32.76±3.49)% and (33.32±4.34)% , respectively; the fecal quantity were (53.20±5.25), (42.40±4.55), (47.10±5.36), (49.50±5.10) and (50.10±5.04) grains, respectively. Compared model group with blank group, and compared experimental-L, -M, -H groups with model group, the above indicators showed statistically significant differences (P<0.05, P<0.01, P<0.001). The relative expression levels of DRD2 mRNA in blank, model and experimental-L, M, H groups were 1.00±0.12, 2.95±0.47, 2.73±0.49, 2.17±0.35 and 2.08±0.32, respectively. The relative expression levels of DRD2 mRNA in the experimental-M and experimental-H groups were significantly lower than those in the model group (all P<0.001), with no significant difference between the two groups (P>0.05); therefore, experimental-M was selected for subsequent experiments. The VIP levels of blank group, model group, experimental-M group, AAV9-NC group and AAV9-DRD2 group were (43.15±4.52), (64.42±7.64), (51.68±5.37), (49.25±4.44) and (56.84±6.41) ng·L^-1, respectively; NO levels were (6.84±0.71), (11.68±1.37), (9.28±0.93), (9.35±0.97) and (10.45±1.03) μmol·L^-1, respectively; the relative expression levels of AMPK protein were 1.00±0.15, 2.42±0.34, 1.68±0.17, 1.55±0.18 and 1.94±0.21, respectively; the relative expression levels of eNOS protein were 1.00±0.11, 3.18±0.35, 2.28±0.23, 2.35±0.27 and 2.95±0.33, respectively. Compared model group with blank group, compared experimental-M group with model group, and compared AAV9-DRD2 group with AAV9-NC group, the above indicators all showed statistically significant differences (all P<0.05).

NOB can improve STC in rats, possibly by down-regulating DRD2 expression, regulating VIP and NO levels, and inhibiting the AMPK/eNOS signaling pathway.

To explore the effects and mechanism of shionone on ulcerative colitis in rats based on the extracellular regulated protein kinase (ERK)/NOD-like receptor protein 3 (NLRP3)/interleukin (IL)-1β signaling pathway.

A total of 60 rats were randomly divided into normal group, model group, experimental-L group, experimental-H group and activator group by random number table method, with 12 rats in each group. The normal group was given drinking water without dextran sulfate sodium, while the other groups were fed with drinking water containing 5% dextran sulfate sodium for 10 days to establish ulcerative colitis rat models. After modeling, rats were administered for 7 days. The experimental-L and -H groups were intragastrically given 50 and 100 mg·kg^-1 shionone daily, respectively; the activator group was intragastrically given 100 mg·kg^-1 shionone daily combined with intraperitoneal injection of 4 mg·kg^-1 ERK activator RO 67-7476; the normal group and model group were intragastrically given and intraperitoneally injected with equal volumes of normal saline daily. Disease activity index was analyzed; the levels of IL-17 and IL-23 in colon tissue were detected by enzyme-linked immunosorbent assay (ELISA); colonic histopathological changes were observed by hematoxylin-eosin (HE) staining; intestinal mucosa was detected by Alcian blue-periodic acid-Schiff (AB-PAS) staining; the relative expression levels of phosphorylated (p)-ERK, NLRP3 and IL-1β proteins were determined by Western blot.

Rats in the model group showed severe colonic tissue damage, characterized by disappearance of intestinal mucosa, blurred epithelial cell structure, gland atrophy, inflammatory cell infiltration, lamellar necrosis of the colonic mucosal layer and decreased number of goblet cells. The disease activity index scores in the normal group, model group, experimental-L group, experimental-H group and activator group were (0.12±0.02), (2.98±0.34), (1.76±0.19), (0.55±0.07) and (2.69±0.29) points, respectively; the levels of IL-17 in colon tissue were (24.64±2.74), (39.78±4.27), (32.92±3.65), (26.13±2.85) and (37.85±3.98) pg·mL^-1, respectively; the levels of IL-23 in colon tissue were (14.25±1.73), (28.47±3.04), (22.14±2.42), (15.96±1.87) and (26.95±2.94) pg·mL^-1, respectively; the histopathological scores of colon tissue were (0±0), (3.73±0.39), (2.49±0.28), (1.24±0.15) and (3.61±0.38) points, respectively; the p-ERK/ERK in colon tissue were 0.32±0.04, 0.81±0.09, 0.58±0.07, 0.36±0.05 and 0.77±0.08, respectively; the relative expression levels of NLRP3 protein were 1.03±0.11, 2.05±0.23, 1.64±0.18, 1.24±0.14 and 1.95±0.22, respectively; the relative expression levels of IL-1β protein were 1.05±0.11, 1.96±0.22, 1.58±0.17, 1.21±0.13 and 1.91±0.21, respectively. Statistical significance was observed in the above indicators when comparing the normal group with the model group, comparing the model group with the experimental-L, H groups and comparing the experimental-H group with the activator group (all P<0.05).

Shionone has protective effects on rats with ulcerative colitis by inhibiting the ERK/NLRP3/IL-1β signaling pathway.

To explore the mechanism of action by which icariin regulates the loss of immune tolerance to immune thrombocytopenia (ITP) through the microRNA (miRNA)-98-5p-mediated adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/Unc-51-like autophagy-activating kinase 1 (ULK1) signaling pathway.

The ITP model was established by intraperitoneal injection of guinea pig anti-mouse platelet serum into mice. Another 12 normal mice were taken as the control group. The mice with successful modeling were divided into model group, the experimental-low group, the experimental-high group and the positive drug group. The experimental-low and experimental-high groups and the positive drug group were gavaged with 1.25, 5.00 mg·kg^-1 icariin and 9.1 mg·kg^-1 prednisone acetate, respectively, after the mice were modeled. The levels of platelets (PLT) and hemoglobin (Hb) were detected by automatic blood analyzer; the levels of thrombopoietin (TPO) and inflammatory factors were detected by enzyme-linked immunosorbent assay; the pathological damage of spleen tissue was detected by hematoxylin-eosin staining; megakaryocytes were observed with sternum bone marrow smears; the relative expression level of miRNA-98-5p was detected by real-time fluorescence quantitative polymerase chain reaction; and the protein relative expression levels of the AMPK/mTOR/ULK1 signaling pathway was detected by Western blotting.

The PLT levels in control group, model group, experimental-low group, experimental-high group and positive drug group were (1 504.56±166.99), (752.68±80.33), (862.95±98.33), (1 212.35±134.23) and (1 363.23±155.33)×10·L^-1, respectively; the Hb levels were (151.33±18.96), (124.11±13.56), (138.32±14.02), (145.33±16.88) and (149.22±16.02) g·L^-1, respectively; the TPO levels were (12.05±1.33), (5.86±0.78), (6.62±0.96), (7.85±0.92) and (9.66±0.89) pg·mL^-1, respectively; the levels of interleukin-6 (IL-6) were (18.96±2.33), (44.33±5.39), (39.25±4.46), (32.32±4.33) and (22.98±3.78) ng·L^-1, respectively; the levels of IL-10 were (42.15±6.48), (23.12±3.56), (26.89±3.99), (31.02±4.65) and (33.66±4.86) ng·L^-1, respectively; the levels of tumor necrosis factor-α(TNF-α) were (31.02±4.65), (77.36±8.98), (67.65±7.88), (60.52±7.34) and (40.56±5.99) ng·L^-1, respectively; the levels of interferon-gamma (IFN-γ) were (4.33±0.68), (8.33±0.96), (7.35±0.89), (6.02±0.81) and (5.86±0.75) ng·L^-1, respectively; the relative expression levels of miRNA-98-5p were 1.00±0.16, 1.78±0.21, 1.51±0.18, 1.22±0.16 and 1.15±0.15, respectively; the relative expression levels of phosphorylated (p)-AMPK/AMPK were 1.00±0.14, 1.81±0.28, 1.60±0.19, 1.31±0.16 and 1.25±0.21, respectively; the relative expression levels of p-mTOR/β-actin were 1.00±0.16, 0.48±0.07, 0.59±0.09, 0.79±0.12 and 0.82±0.14, respectively; the relative expression levels of p-ULK1/β-actin were 1.00±0.15, 0.42±0.06, 0.53±0.09, 0.89±0.14 and 0.93±0.16, respectively. There were statistically significant differences when comparing the above indicators of model group with those of control group, and also when comparing the above indicators of the experimental-low, experimental-high groups and positive drug group with those of model group (P<0.05, P<0.01, P<0.001).

Icariin regulates the loss of immune tolerance in rats with ITP, inhibits autophagy, and thus elevates platelet levels by down-regulating the expression of miRNA-98-5p and modulating the AMPK/mTOR/ULK1 signaling pathway.

To investigate the effects of bicalutamide (BIC) on the malignant biological behavior of prostate cancer LNCaP cells through cadherin 7 (CDH7), and to explore its possible mechanism of action.

This study was divided into two parts, animal experiment and cell experiment. In animal experiment, 30 Balb/c male nude mice were randomly divided into animal blank control group (daily gavage of 10 mL·kg^-1 0.5% carboxymethyl cellulose sodium solution), animal positive control group (daily gavage of 10 mL·kg^-1 enzalutamide) and animal experimental group (daily gavage of 25 mg·kg^-1 BIC), with 10 nude mice in each group. All mice were treated with subcutaneous injection of LNCaP cell suspension to establish a xenograft model and each group was continuously treated for 28 days. The tumor volume of nude mice in each group was recorded every 7 days; tumor tissues were collected 24 h after drug withdrawal; the expression of proliferating cell nuclear antigen (PCNA) protein was detected by immunohistochemistry. In cell experiment, LNCaP cells were divided into cell blank control group (normal culture, no treatment), cell positive control group (treated with enzalutamide 1 μM), cell experimental group (treated with BIC 50 μM), oe-NC group (transfected with oe-NC plasmid and then treated with BIC 50 μM), and oe-CDH7 group (transfected with oe-CDH7 plasmid and then treated with BIC 50 μM). The relative expression levels of CDH7 mRNA in cells was detected by real-time fluorescence quantitative polymerase chain reaction method. The cell invasion ability and apoptosis rate were detected by Transwell assay and terminal-deoxynucleotidyl transferase mediated nick end labeling method, respectively. The activities of superoxide dismutase (SOD) and the levels of malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay. The relative expression levels of CDH7 and proteins related to relevant pathways were detected by Western blot.

In animal experiments, the tumor volume on day 21 of animal blank control group, animal positive control group and animal experimental group were (622.30±131.15), (411.90±72.07) and (467.40±63.92) mm³, respectively; the tumor volumes on day 28 were (1 189.50±225.95), (729.40±142.90) and (688.60±89.07) mm³, respectively; and the relative expression levels of PCNA protein were 1.00±0.11, 0.28±0.09 and 0.33±0.07, respectively. There were statistically significant differences compared animal positive control group or animal experimental group with the control group (all P<0.001). In cell experiments, the relative expression levels of CDH7 mRNA in the cell blank control group, cell positive control group, cell experimental group, oe-NC group and oe-CDH7 group were 1.00±0.16, 0.35±0.07, 0.40±0.05, 0.37±0.05 and 3.12±0.34, respectively; the number of cell invasions were (134.26±24.97), (57.63±11.53), (66.34±11.84), (61.17±9.12) and (98.08±15.88) pieces, respectively; the MDA levels were (126.94±20.81), (257.63±46.19), (239.21±29.32), (244.35±38.46) and (187.79±25.35) pg·mL^-1, respectively; the apoptosis rates were (4.54±0.87)%, (53.27±6.14)%, (47.13±7.15)%, (51.76±9.59)% and (17.49±3.48) %, respectively; the relative expression levels of extracellular signal-regulated kinase 1/2 (ERK1/2) protein were 1.00±0.12, 0.44±0.06, 0.39±0.05, 0.41±0.03 and 0.67±0.11, respectively. Compared cell positive control group, or cell experimental group with cell blank control group, compared oe-CDH7 group with oe-NC group, the above indicators were all statistically significantly different (all P<0.001).

BIC could inhibit the invasion of prostate cancer LNCaP cells and promote their apoptosis through CDH7, and the mechanism of action may be related to the inhibition of mitogen-activated protein kinase (MAPK)-ERK signaling pathway activation.