To observe the clinical efficacy and safety of bevacizumab injection combined with paclitaxel injection and carboplatin injection in the treatment of patients with advanced ovarian cancer.

Patients with advanced ovarian cancer were randomly divided into control group and treatment group. The control group was given 175 mg·m^-2 paclitaxel once every 3 weeks, the intravenous infusion was not less than 3 h + 0.3 - 0.4 g·m^-2 carboplatin once every 3 weeks, intravenous infusion. On the basis of control group, the treatment group was given 15 mg·kg^-1 bevacizumab once every 3 weeks, intravenous infusion. Two groups were treated for 6 courses with 3 weeks per course. The clinical efficacy, tumor markers, vascular related factors, T lymphocyte and miRNA-30 levels, survival during treatment and safety were compared between two groups.

Treatment group was enrolled 71 cases, 10 cases dropped out, and 61 cases were finally included in the statistical analysis. Control group was enrolled 70 cases, 10 cases dropped out, and 60 cases were finally included in the statistical analysis. After treatment, the disease remission rates of treatment and control groups were 60.66% (37 cases/61 cases) and 41.67% (25 cases/60 cases) with statistically significant difference (P<0.05). After treatment, the cluster of differentiation 133 levels were (11.44±2.46) and (26.77±5.41) U·mL^-1, the DEAD-box helicase 4 levels were (13.55±3.48) and (33.16±5.46) U·mL^-1, the relative expression levels of miRNA-30b were 1.03±0.07 and 1.15±0.08, the relative expression levels of miRNA-30c were 1.09±0.05 and 1.22±0.06, the differences were statistically significant (all P<0.05). During follow-up, all-cause deaths of treatment and control groups were 8 and 11 cases, the survival rates were 86.89% and 81.67% (all P>0.05). The adverse drug reactions in both groups were mainly gastrointestinal reactions, alopecia, allergies and liver dysfunction. The total incidences of adverse drug reactions in the treatment and control groups were 55.74% and 43.33%, without significant difference (P>0.05).

Bevacizumab injection combined with paclitaxel injection and carboplatin injection has better clinical efficacy in the treatment of patients with advanced ovarian cancer than paclitaxel injection combined with carboplatin injection, the former can significantly reduce the levels of tumor markers, improve immune function, without increasing the incidence of adverse drug reactions.

To investigate the influencing factors of the dose-corrected concentration (C/D) of the active metabolite of oxcarbazepine (OXC) [10-hydroxycarbazepine (MHD)] and to provide the reference for the rational clinical use of this drug.

A total of 161 MHD blood concentrations were collected from the therapeutic drug monitoring (TDM) data of inpatients who received OXC treatment, as well as demographic information, comedications, diagnosis, and associated clinical chemistry results. Data analysis was carried out through the SPSS 27.0 software.

The effects of age, body mass index (BMI), comedications and diagnosis on MHD C/D values were statistically significant (all P<0.05). The C/D value of patients under 18 years old was higher than that of patients between 18 to 65 years old. The C/D value of female patients was higher than that of male patients in adults. The C/D value of the underweight group was higher than the normal, overweight and obese groups. The C/D value of patients combined with valproic acid was significantly lower than that of patients who didn’t. The C/D value of epilepsy patients was significantly lower than that of patients who weren’t diagnosed with this disease. Only 11 patients (8.20%) had blood sodium below the normal value range after medication, and there was no significant difference in blood sodium value, serum creatinine value, and glutamic-pyruvic transaminase value before and after treatment (all P>0.05). The results of multiple linear regression analysis showed that BMI had an effect on the C/D of MHD (P<0.05).

OXC has relatively good safety profile, and the effects of gender, age, BMI, comedications and diagnosis should be taken into consideration when OXC is prescribed.

To investigate the effect of inhibition of mitochondrial pyruvate carrier on Okada-induced cuprotosis in SH-SY5Y cells.

SH-SY5Y cells were induced by okada acid (OA) to establish a model of Alzheimer’s disease (AD). The cells were divided into control group (complete medium), model group (20 nmol·L^-1 OA) and experimental group [20 nmol·L^-1 OA+1 μmol·L^-1 2-cyano-3 -(1-phenyl-1H-indole-3-yl) -2-acrylic acid (UK-5099)]. Copper ion content was detected by cell cupric colorimetric kit. Pyruvate content was detect by pyruvate detection kit, and the expressions of phosphorylated Tau (AT8) and ferredoxin 1 (FDX1) in each group were detected by immunofluorescence staining. The expression levels of mitochondrial pyruvate carrier (MPC1/MPC2) and dihydrolipoyl transacetylase (DLAT) were detected by Western blot.

The contents of copper ions in experimental group, model group and control group were (0.36±0.01), (0.90±0.05) and (0.23±0.04) μmol·g prot^-1; the pyruvate content were (0.55±0.04), (0.33±0.03) and (0.44±0.04) μmol·10⁸ cell^-1; the AT8 expression levels were 91.46±14.53, 125.02±14.43 and 72.57±19.81; the FDX1 expression levels were 98.93±7.40, 147.83±18.63 and 79.18±8.06; the relative expression levels of MPC1 protein were 0.59±0.11, 1.01±0.14 and 0.55±0.13; the relative expression levels of MPC2 protein were 0.54±0.05, 1.31±0.07 and 0.43±0.07; the relative expression levels of DLAT protein were 0.72±0.04, 0.92±0.07 and 0.53±0.14, respectively. The above indexes in the experimental group were statistically significant compared with those in the model group (P<0.05, P<0.01, P<0.001).

Inhibition of mitochondrial pyruvate carrier can alleviate Okada-induced cuprotosis of SH-SY5Y cells.

To achieve overexpression of phosphoglycerate kinase 1 (PGK1) in HEK-293T cells and screen the key site of its succinylation through constructing PGK1 overexpression vector (PGK1-WT) and four lysine site succinylation mutation vectors.

GEPIA2 database was used to analyze the expression of PGK1 mRNA in normal breast tissue (291 cases) and breast cancer tissue (135 cases) and the relationship between PGK1 expression level and the overall survival rate of breast cancer patients. Protein modification proteomics was used to detect the levels of protein succinylation in four triple negative breast cancer (TNBC) cell lines (MDA-MB-436, MDA-MB-468, MDA-MB-231, BT-549) and normal breast epithelial cells (MCF-10A); the succinylated positive and negative mutation vectors of K11, K131, K323, K361 were contructed with point mutation kit. The experiment was divided into NC, shPGK1-496, shPGK1-220, PGK1-WT groups and positive and negative mutant groups of K11, K131, K323 and K361. Real-time fluorescence quantitative polymerase chain reaction was used to detect the level of expression of PGK1 mRNA in NC, shPGK1-496 and shPGK1-220 groups. The expression levels of PGK1 proteins in NC, shPGK1-496 and shPGK1-220 groups, and the expression levels of Flag proteins in NC, PGK1-WT and four sites in positive and negative mutant groups were detected by Western blot. The key site of PGK1 succinylation was detected by co-immunoprecipitation.

Compared with normal breast tissues, the level of PGK1 mRNA was highly expressed in breast cancer tissue, and the survival time of breast cancer patients with high PGK1 expression was shorter. Four lysine sites of PGK1 in TNBC cells were hypersuccinylated. The relative expression levels of PGK1 mRNA in NC, shPGK1-496 and shPGK1-220 groups were 1.03±0.23, 0.15±0.11 and 1.42±0.69, respectively; the relative expression levels of PGK1 protein were 1.08±0.05, 0.49±0.05 and 1.28±0.01 respectively; compared with NC group, the above indexes in shPGK1-496 group were statistically different (all P<0.01). The relative expression levels of Flag protein in NC group, PGK1-WT group and positive and negative mutant groups of K11, K131, K323 site were 0, 3.43±0.09, 3.28±0.10, 2.28±0.11, 3.03±0.03, 2.79±0.11, 3.29±0.09 and 2.98±0.04, respectively; compared with the NC group, PGK1-WT group and the positive and negative mutant groups of K11, K131 and K323 had statistical differences (all P<0.01). The relative expression levels of Flag protein in NC group, PGK1-WT group and K361 positive and negative mutant group were 0, 2.58±0.11, 3.04±0.02 and 4.04±0.10, respectively; compared with NC group, PGK1-WT group and K361 positive and negative mutant group had statistical significance (all P<0.01). The levels of lysine succinylation in IgG group, PGK1-WT group and negative mutant groups of K11, K131, K323, K361 were 0, 1.53±0.12, 1.30±0.18, 1.29±0.09, 1.23±0.03 and 0.89±0.16, respectively; compared with PGK1-WT group, the negativ mutant group of K361 had statistical significance (P<0.01).

The four lysine sites of PGK1 in TNBC cells are highly succinylated, and K361 site is critical to their succinylation.

To explore the mechanism of inhibiting invasion and epithelial mesenchymal transformation of esophageal squamous cell carcinoma cells by chidamide (CHI) through long noncoding RNA (LncRNA) VPS9D1-AS1.

Human normal esophageal epithelial cells (HEEC) group (HEEC were cultured normally without any treatment), human esophageal squamous cell carcinoma KYSE-450 cells were divided into KYSE-450 group (normal culture), CHI group (treated with 20 μmol·L^-1 CHI for 48 h), CHI+oe-NC group (transfected with oe-NC, treated with 20 μmol·L^-1 CHI for 48 h), CHI+oe-LncRNA VPS9D1-AS1 group (transfected with oe-LncRNA VPS9D1-AS1, treated with 20 μmol·L^-1 CHI for 48 h). The positive expression of LncRNA VPS9D1-AS1 in the cells was detected by fluorescence in situ hybridization, the invasion ability of the cells was detected by Transwell, and the epithelial mesenchymal transformation and mitogen-activated protein kinase (MEK)/extracellular signal-related protein kinase (ERK) signaling pathway related protein expression levels were detected by protein Western blot.

The positive expression levels of LncRNA VPS9D1-AS1 in HEEC group, KYSE-450 group and CHI group were 1.00±0.06, 4.58±0.84 and 1.93±0.37, respectively. Compared with HEEC group and KYSE-450 group, compared with CHI group and KYSE-450 group, the positive expression levels of LncRNA VPS9D1-AS1 were significantly different (P<0.05). The invasion numbers of cells in KYSE-450 group, CHI group, CHI+oe-NC group, CHI+oe-LncRNA VPS9D1-AS1 group were 89.57±15.61, 22.49±5.18, 27.04±5.95 and 57.82±10.73, respectively; the relative expression levels of N-cadherin were 1.00±0.07, 0.52±0.12, 0.59±0.09 and 0.91±0.16, respectively; the relative expression levels of E-cadherin were 1.00±0.11, 1.81±0.35, 1.79±0.30 and 1.24±0.22, respectively; the relative expression levels of MEK1 were 1.00±0.08, 0.64±0.11, 0.69±0.13 and 0.93±0.17, respectively; p-ERK1/ERK1 levels were 1.00±0.05, 0.61±0.07, 0.55±0.10 and 0.95±0.15, respectively; p-ERK2/ERK2 levels were 1.00±0.12, 0.43±0.09, 0.42±0.08 and 0.89±0.14, respectively. Compared between KYSE-450 group and CHI group, between CHI+oe-LncRNA VPS9D1-AS1 group and CHI+oe-NC group, there were statistical significance in the levels of the above indexes (P<0.05).

CHI can inhibit esophageal squamous cell invasion and epithelial mesenchymal transformation, which may be related to the inhibition of MEK/ERK signaling pathway activation by LncRNA VPS9D1-AS1 down-regulated by CHI.

To explore the effects of ginsenoside Rh2 on the development of colon cancer through microRNA-128-3p(miR-128-3p)/growth differentiation factor 15(GDF15) mediated wingless-type MMTV integration site family member (Wnt)/β-catenin signaling pathway.

SW620 colorectal cancer cells were randomly divided into the following groups: Control group (standard culture), experimental group (treated with ginsenoside Rh2 at 20 μmol·L^-1), NC inhibitor group (transfected with NC inhibitor), miR-128-3p inhibitor group (transfected with miR-128-3p inhibitor), ginsenoside Rh2 + miR-128-3p inhibitor group (treated with ginsenoside Rh2 at 20 μmol·L^-1 and transfected with miR-128-3p inhibitor), and ginsenoside Rh2+miR-128-3p inhibitor+si-GDF15 group (treated with ginsenoside Rh2 at 20 μmol·L^-1, transfected with miR-128-3p inhibitor and si-GDF15). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of miR-128-3p and GDF15 mRNA. Cell proliferation was assessed using 5-ethynyl-2′-deoxyuridine (EdU) incorporation assay. Western blotting was employed to detect the protein relative levels of myelocytomatosis oncogene (Myc) and β-catenin.

The relative expression levels of miR-128-3p in the control group and experimental group were 1.00±0.16 and 1.56±0.25, respectively; the relative expression relative levels of GDF15 mRNA were 1.00±0.12 and 0.43±0.05, respectively; the proliferation rates were (88.76±8.56)% and (35.89±4.05)%, respectively; the v-myc avian myelocytomatosis viral oncogene homolog (Myc) protein levels were 1.00±0.21 and 0.45±0.06, respectively; and the β-catenin protein relative levels were 1.00±0.23 and 0.52±0.07, respectively. Compared with the control group, the above indicators in the experimental group showed statistically significant differences (all P<0.05). In the ginsenoside Rh2+miR-128-3p inhibitor group and ginsenoside Rh2+miR-128-3p inhibitor+si-GDF15 group, the cell proliferation rates were (68.56±7.12)% and (50.56±5.18)%, respectively; the Myc protein relative levels were 0.86±0.12 and 0.61±0.08, respectively; and the β-catenin protein relative levels were 0.71±0.09 and 0.58±0.08, respectively. The above indicators in the ginsenoside Rh2+miR-128-3p inhibitor group compared with the experimental group, and those in the ginsenoside Rh2+miR-128-3p inhibitor+si-GDF15 group compared with the ginsenoside Rh2+miR-128-3p inhibitor group, all showed statistically significant differences (all P<0.05).

Ginsenoside Rh2 can inhibit the proliferation and migration of colon cancer SW620 cells, and promote the apoptosis, which may be related to the regulation of ginsenoside Rh2 on the miR-128-3p/GDF15 to inhibit Wnt/β-catenin signaling pathway.

To investigate the effects of pitavastatin on lipopolysaccharide (LPS)-induced H9c2 cells and its mechanism.

H9c2 cells were divided into control group, model group (treated with 10 μg·mL^-1 LPS), experimental group (after 1 μmol·L^-1 pitavastatin treatment, 10 μg·mL^-1 LPS treatment), and combination group [treated with 1.28 μmol·L^-1 NLR family pyrin domain containing protein 3 (NLRP3) agonist on the basis of experimental group]. The NLRP3/cysteine-requiring aspartate protease 1 (caspase-1)/gasdermin D (GSDMD) signaling pathway related protein levels were detected by Western blot. The messenger ribonucleic acid (mRNA) relative expression levels related to inflammation and mitochondrial function were detected by quantitative real time polymerase chain reaction.

The relative expression levels of NLRP3 protein in control group, model group, experimental group and combination group were 1.00±0.15, 2.56±0.38, 1.35±0.19 and 2.15±0.31, respectively; the relative expression levels of caspase-1 protein were 1.00±0.18, 1.88±0.22, 1.22±0.20 and 1.75±0.22, respectively; the relative expression levels of GSDMD protein were 1.00±0.14, 2.12±0.32, 1.55±0.21 and 1.99±0.23, respectively; the relative expression levels of tumor necrosis factor-α mRNA were 1.00±0.15, 4.12±0.65, 2.11±0.29 and 3.54±0.48, respectively; the relative expression levels of interleukin-1β mRNA were 1.00±0.18, 3.33±0.39, 1.42±0.25 and 2.23±0.33, respectively; the relative expression levels of interleukin-18 mRNA were 1.00±0.14, 2.28±0.28, 1.33±0.26 and 1.98±0.22, respectively; the relative expression levels of PPAR-γ coactivator 1 alpha (PGC-1α) mRNA were 1.00±0.14, 0.45±0.07, 0.89±0.12 and 0.61±0.08, respectively; the relative expression levels of mitochondrial transcription factor A mRNA were 1.00±0.19, 0.53±0.07, 0.77±0.09 and 0.58±0.08, respectively; the relative expression levels of nuclear respiratory factor-1 mRNA were 1.00±0.17, 0.62±0.08, 0.85±0.13 and 0.65±0.08, respectively; the relative expression levels of uncoupling protein 2 mRNA were 1.00±0.15, 0.34±0.05, 0.92±0.16 and 0.48±0.07, respectively. The above indexes in model group were compared with those in control group, those in experimental group were compared with those in model group, and those in combination group were compared with those in experimental group, the differences were statistically significant (all P<0.05).

Pitavastatin can inhibit inflammation, reduce pyroptosis of H9c2 cells, and protect mitochondrial function, which may be achieved by inhibiting the NLRP3/caspase-1/GSDMD signaling pathway.

To investigate the protective effects and potential mechanisms of 6-gingerol against acute respiratory distress syndrome (ARDS) in juvenile mice through nerve growth factor-induced clone B (Nur77).

The juvenile mouse model of ARDS was established by tracheal instillation of lipopolysaccharide. After modeling, 48 juvenile mice were randomly divided into the model group, the 6-gingerol group (intraperitoneal injection of 30 mg·kg^-1 6-gingerol), the 6-gingerol+sh-NC group (intranasal instillation of sh-NC negative control adenovirus+intraperitoneal injection of 30 mg·kg^-1 6-gingerol), and the 6-gingerol+sh-Nur77 group (intranasal instillation of sh-Nur77 adenovirus+intraperitoneal injection of 30 mg·kg^-1 6-gingerol). Another 12 normal juvenile mice were given an equal volume of sterile 0.9% NaCl by tracheal instillation as the sham operation group. Detected the lung wet/dry (W/D) ratio of young mice in each group. The immunohistochemistry method was used to detect the positive expression of collagen Ⅲ in lung tissues. The kit was used to detect apoptosis in the lung tissues of young mice. The expressions of pathway-related proteins were detected by Western blotting.

The W/D ratios of the sham operation group, the model group, the 6-gingerol group, the 6-gingerol+sh-NC group and the 6-gingerol+sh-Nur77 group were 2.20±0.26, 6.65±0.92, 3.89±0.52, 3.72±0.44 and 5.55±0.78, respectively; the positive levels of collagen Ⅲ were 1.00±0.22, 3.99±0.54, 1.85±0.28, 1.76±0.29 and 2.79±0.34, respectively; the apoptosis rates were (4.65±0.66)%, (39.62±5.03)%, (18.63±2.33)%, (17.82±2.12)% and (33.65±5.03)%, respectively; the levels of phosphorylated phosphatidylinositol 3-kinase/phosphatidylinositol 3-kinase (p-PI3K/PI3K) were 1.00±0.13, 1.66±0.22, 1.23±0.17, 1.21±0.14 and 1.58±0.24, respectively; the levels of phosphorylated protein kinase B/protein kinase B (p-Akt/Akt) were 1.00±0.16, 1.78±0.26, 1.33±0.21, 1.38±0.19 and 1.60±0.22, respectively. Compared with the sham operation group, the differences in the above indicators of the model group were statistically significant (all P<0.05); compared with the model group, the differences in the 6-gingerol group were statistically significant (all P<0.05); compared with the 6-gingerol+sh-NC group, the differences in the 6-gingerol+sh-Nur77 group were also statistically significant (all P<0.05).

6-gingerol intervention can improve lung injury in young ARDS mice, up-regulate the expression of Nur77, inhibit lung tissue inflammatory response, reduce lung tissue apoptosis, and promote coagulation/fibrinolytic balance, and its mechanism of action may be related to the inhibition of PI3K/Akt pathway.

To investigate the effects of paeoniflorin on insulin resistance and myocardial injury in rats with gestational diabetes mellitus and its mechanism.

Female rats were randomly divided into control group (normal diet), model group [male rats fed with high-fat diet and intraperitoneally injected 30 mg·kg^-1 streptozotocin (STZ) after close cages], experimental group (after modeling, 50 mg·kg^-1 paeoniflorin was given by gavage), si-NC group (50 mg·kg^-1 paeoniflorin + si-NC plasmid injected into tail vein after modeling), si-IGFBP2 group (50 mg·kg^-1 paeoniflorin + si-IGFBP2 plasmid injected into tail vein after modeling), each group of 10 rats. After 2 weeks of continuous treatment, fasting blood glucose (FBG) was measured with a glucose meter. Serum insulin-like growth factor binding protein 2 (IGFBP2), fasting insulin (FINS), cardiac troponin Ⅰ (cTnⅠ), creatine kinase isoenzyme MB (CK-MB) related factors were detected by enzyme-linked immunosorbent assay (ELISA), insulin resistance index (HOMA-IRI) was calculated, and the expression of signal pathway-related proteins was detected by Western blot assay.

The levels of FBG in control group, model group, experimental group, si-NC group and si-IGFBP2 group were: (5.62±0.56), (18.10±1.76), (9.81±1.46), (10.02±1.38) and (16.32±1.87) mmol·L^-1, respectively; IGFBP2 levels were (39.47±2.64), (20.65±1.86), (27.18±1.85), (27.95±1.74) and (15.28±1.22) ng·mL^-1, respectively; FINS levels were (8.72±0.75), (21.11±2.50), (16.88±1.86), (16.06±1.39) and (20.01±2.94) mU·L^-1, respectively; cTnⅠ levels were (406.04±29.98), (788.11±84.43), (513.70±57.62), (526.85±38.03) and (756.51±63.88) pg·mL^-1, respectively; CK-MB levels were (7.98±0.07), (15.15±1.26), (11.59±1.23), (11.37±1.79) and (13.49±1.54) U·L^-1, respectively; HOMA-IRI levels were 2.17±0.26, 16.92±2.12, 6.24±0.95, 6.60±1.10 and 12.83±1.68, respectively; the relative expression levels of phosphorylate-phosphatidylinositol 3-kinase (p-PI3K) protein were 0.68±0.11, 0.39±0.04, 0.53±0.05, 0.51±0.06 and 0.43±0.04, respectively; the above indexes in the model group were compared with the control group, the experimental group were compared with the model group, and the si-IGFBP2 group were compared with the si-NC group, the differences were statistically significant (all P<0.05).

Paeoniflorin may improve insulin resistance and myocardium injury in gestational diabetes mellitus rats by up-regulating IGFBP2 expression.

To explore the effects of rapamycin (RAP) combined with cyclosporine A (CsA) on the hematopoietic function and the levels of bone marrow vascular endothelial growth factor (VEGF), thrombopoietin (TPO), and vascular cell adhesion molecule-1 (VCAM-1) in aplastic anemia mice by regulating the T-box transcription factor (T-bet)/interferon-gamma (IFN-γ) signaling pathway.

Female Kunming mice of pure line were randomly divided into control group (without any treatment), model group (subcutaneously injected with 50 mg·kg^-1 cyclophosphamide, once every other day for a total of 4 times; meanwhile, inhaling 30 mg·L^-1 toluene once a day for 8 consecutive days), CsA group (intraperitoneally injected with 5 mg·kg^-1 CsA on the basis of the model group), RAP-L combined with CsA group (intraperitoneally injected with 5 mg·kg^-1 CsA and 0.1 mg·kg^-1 RAP on the basis of the model group), RAP-M combined with CsA group (intraperitoneally injected with 5 mg·kg^-1 CsA and 0.5 mg·kg^-1 RAP on the basis of the model group), RAP-H combined with CsA group (intraperitoneally injected with 5 mg·kg^-1 CsA and 1 mg·kg^-1 RAP on the basis of the model group), and RAP-H group (intraperitoneally injected with 1 mg·kg^-1 RAP on the basis of the model group), with 10 mice in each group. Except for the control group, the aplastic anemia model was established in the other groups. A biochemical analyzer was used to detect the levels of peripheral blood red blood cells (RBC), white blood cells, hemoglobin and platelets. Hematoxylin-eosin staining was used to observe the bone marrow morphology and conduct pathological injury scoring. The enzyme-linked immunosorbent assay method was used to detect the levels of VEGF, VCAM-1, TPO, IFN-γ and tumor necrosis factor-α in the bone marrow supernatant. Immunohistochemistry was used to detect the expression of TPO. Real-time fluorescence quantitative polymerase chain reaction and Western blotting were used to detect the messenger ribonucleic acid (mRNA) and protein expressions of T-bet in bone marrow mononuclear cells.

The RBC levels of the control group, model group, CsA group, RAP-H combined with CsA group and RAP-H group were (8.48±0.89)×10¹², (2.14±0.25)×10¹², (3.54±0.54)×10¹², (6.12±0.74)×10¹² and (3.26±0.61) ×10¹²·L^-1, respectively; the pathological injury scores were (0.20±0.04), (2.50±0.25), (1.10±0.10), (1.00±0.11) and (1.20±0.16) points, respectively; the TPO levels were (195.48±28.15), (145.81±15.24), (169.76±20.26), (190.54±22.37) and (165.52±20.29) pg·mL^-1, respectively; the VCAM-1 levels were (213.46±32.33), (132.81±21.94), (185.49±19.65), (204.19±19.82) and (183.67±20.87) ng·mL^-1, respectively; the IFN-γ levels were (132.04±18.10), (232.46±25.29), (205.98±21.26), (183.67±20.20) and (209.05±19.82) pg·mL^-1, respectively; the relative expression levels of T-bet mRNA were 1.00±0.10, 3.98±0.69, 2.18±0.21, 1.95±0.20 and 2.24±0.23, respectively; the relative expression levels of T-bet protein were 1.00±0.10, 2.46±0.29, 1.98±0.21, 1.67±0.20 and 2.01±0.22, respectively. When the above-mentioned indicators of the model group were compared with those of the control group, the above-mentioned indicators of the CsA group, the RAP-H combined with CsA group, and the RAP-H group were compared with those of the model group, and the above-mentioned indicators of the RAP-H combined with CsA group were compared with those of the CsA group and the RAP-H group, all the differences were statistically significant (all P<0.05).

CsA combined with RAP can significantly improve the hematopoietic function and cellular immune function of aplastic anemia model mice, which may be related to increasing the levels of bone marrow TPO and VCAM-1 and regulating the T-bet/IFN-γ signaling pathway.