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 evaluate the bioequivalence of test preparation (T) and reference preparation (R) of diphenidol hydrochloride tablets taken orally in a single fasting/postprandibular state in healthy Chinese subjects.

This protocol was designed as random, open, single-center, single-dose, double-cycle and double-cross experiment was selected in this study. A total of 66 healthy male and female subjects were enrolled, including 24 subjects in the test group and 42 subjects in the reference group. All subjects took the test preparation and the reference preparation 25 mg in each cycle. The plasma concentration of diphenidol hydrochloride was determined by high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS), and the pharmacokinetic (PK) data collected was analyzed and processed statistically.

The PK parameters of diphenidol hydrochloride tablets and reference preparations in fasting group were as follows: C_max were (75.90±34.60) and (67.96±19.90) ng·mL^-1, respectively; AUC_0-t were (387.67±198.48) and (341.57±137.05) ng·h·mL^-1, respectively; AUC_0-∞ were (413.00±228.39) and (361.70±161.19) ng·h·mL^-1, respectively. Main PK parameters of diphenidol hydrochloride tablets and reference preparations orally taken by subjects after meals: C_max were (92.60±33.60) and (85.30±31.96) ng·mL^-1, respectively; AUC_0-t were (511.90±206.87) and (498.33±197.78) ng·h·mL^-1, respectively; AUC_0-∞ were (543.21±236.90) and (513.98±203.92) ng·h·mL^-1, respectively. Under fasting and postprandial conditions, subjects took diphenidol hydrochloride tablet and reference preparation orally, one tablet 25 mg each time. The geometric mean of the main pharmacokinetic parameters of difenidol in plasma (C_max, AUC_0-t, AUC_0-∞) and the ratio of their corresponding parameters ranged from 80.00% to 125.00% with 90% confidence interval, and no serious adverse events occurred in both groups.

Diphenidol hydrochloride tablets show bioequivalence and good safety evaluation under fasting and postprandial conditions

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 whether the supplemented Buyang Huanwu tang can improve the kidney injury in diabetic kidney disease (DKD) mice through regulating mitochondrial dynamics.

The db/db mice were randomized into the model group (0.2 mL·d^-1 distilled water), low and high-dose experimental groups (16.0, 32.0 g·kg^-1 supplemented Buyang Huanwu tang), with 8 mice in each group. Another 8 db/m mice were included in the normal group (0.2mL·d^-1 distilled water). The four groups were orally administered once a day for 8 consecutive weeks. Then, the levels of fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG), blood urea nitrogen (BUN), serum creatinine (SCr), and urinary microalbumin (mALB) were detected at the end of the experiment. The expression of mitofusin 1 (Mfnl), mitofusin 2 (Mfn2), optic atrophy 1 (Opa1), dynamin-related protein 1 (Drp1), fission protein 1 (Fis1), sirtuin 3 (SIRT3), transforming growth factor-β₁ (TGF-β₁), α-smooth muscle actin (α-SMA), collagen type Ⅲ (Col-Ⅲ) and fibronectin (FN) was measured by Western blotting.

The levels of TG in the experimental-L, -H groups, model group and normal group were (1.98±0.13), (1.69±0.13), (3.38±0.59) and (1.25±0.16) mmol·L^-1; the levels of TC were (3.86±0.14), (3.19±0.15), (5.41±0.61) and (1.46±0.19) mmol·L^-1; the levels of BUN were (10.04±2.21), (8.79±1.75), (16.92±4.57) and (4.78±1.07) mmol·L^-1; the levels of SCr were (19.17±2.25), (17.16±2.03), (27.92±4.13) and (13.37±1.77) μmol·L^-1; the levels of mALB were (26.92±4.61), (20.54±2.31), (46.78±7.32) and (6.14±1.13) mg·L^-1; the relative expression levels of TGF-β1 were 0.73±0.09, 0.59±0.05, 1.01±0.14 and 0.48±0.05; the relative expression levels of α-SMA were 0.79±0.09, 0.56±0.05, 1.12±0.11 and 0.55±0.04; the relative expression levels of FN were 0.61±0.03, 0.55±0.05, 0.83±0.09 and 0.22±0.03; the relative expression levels of Col-Ⅲ were 0.53±0.06, 0.35±0.05, 0.73±0.09 and 0.17±0.03; the relative expression levels of SIRT3 were 0.65±0.07, 0.41±0.14, 0.23±0.12 and 0.91±0.04; the relative expression levels of Drp1 were 0.54±0.08, 0.49±0.09, 0.98±0.11 and 0.37±0.03; the relative expression levels of Fis1 were 0.71±0.05, 0.51±0.03, 1.14±0.11 and 0.35±0.05; the relative expression levels of Mfn1 were 0.61±0.04, 0.95±0.05, 0.43±0.05 and 1.02±0.07; the relative expression levels of Mfn2 was 0.67±0.06, 0.89±0.09, 0.52±0.03 and 1.08±0.05; the relative expression levels of OPA1 were 0.77±0.06, 0.79±0.09, 0.52±0.03 and 1.13±0.11, respectively. Significant differences were found between the model group and experimental-L, -H groups (P<0.05, P<0.01). Simultaneously, the renal pathological and mitochondrial damage was significantly improved.

The supplemented Buyang Huanwu tang can maintain the balance of mitochondrial dynamics, thereby reducing urinary protein, alleviating renal injury and fibrosis. Its potential mechanism may be related to the regulation of SIRT3 protein expression.

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 protective effects of orphan nuclear receptor subfamily 2 group E member 1 (NR2E1) overexpression on nerve regeneration in dentate gyrus (DG) of diabetic rats complicated with depression.

The rat model of diabetes complicated with depression was established by injecting streptozotocin into the tail vein combined with chronic unpredictable mild stimulation. The successful rats were randomly divided into model, control and experimental groups, with 8 rats per group; another 8 normal rats were set as normal group. Control group was injected adeno-associated control virus 4 μL. Experimental group was injected with adeno-associated virus of overexpress NR2E1 4 μL; model and normal groups were injected with 0.9% NaCl. After 14 days, the depression-like behavior of rats was detected by Morris water maze, the fasting blood glucose level was detected by blood glucose meter, and the serum insulin (INS), interleukin -1β (IL-1β) and tumor necrosis factor-α (TNF-α) levels in DG area were detected by enzyme-linked immunosorbent assay. The expression of thymidine analogue bromodeoxyuridine (Brdu) in DG region was detected by immunofluorescence method, and the signal transduction expression levels of microRNA-let-7d (miRNA-let-7d)/NR2E1/silencing information regulatory factor 1 (SIRT1) gene were detected by real-time fluorescence quantitative polymerase chain reaction.

The space exploration time of experimental, control, model and normal groups was (31.25±9.94), (25.50±8.02), (19.75±5.82) and (43.87±12.77) s; the fasting blood glucose were (19.28±3.60), (25.26±5.25), (23.71±4.13) and (4.45±0.40) mmoL·L^-1; the insulin levels were (77.15±3.03), (80.53±4.93), (83.31±5.77) and (48.15±5.18) ng·mL^-1; the IL-1β levels were (28.15±4.68), (36.83±6.97), (40.18±4.40) and (19.15±2.67) pg·mL^-1; the TNF-α levels were (281.15±25.15), (324.06±16.85), (337.08±23.11) and (219.06±27.68) pg·mL^-1; the integrated optical density of Brdu were 1.70±1.19, 0.89±0.12, 0.93±0.14 and 2.14±0.15; the relative expression levels of miRNA-let-7d were 2.02±0.18, 2.67±0.54, 2.88±0.30 and 1.11±0.16; the relative expression levels of NR2E1 mRNA were 2.87±0.39, 0.96±0.09, 1.07±0.12 and 3.29±0.35; the relative expression levels of SIRT1 mRNA were 1.62±0.37, 0.99±0.08, 1.04±0.10 and 2.30±0.34, respectively. Compared with the model group, the above indexes in experimental group have statistical significance (all P<0.05).

The overexpression of NR2E1 receptor in isolated nucleus may protect the dentate gyrus nerve regeneration in diabetic rats with depression by regulating miRNA-let-7d/TLX/SIRT1 signal transduction.

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.

To observe clinical effect and safety of dapagliflozin tablets combined with metformin tablets in the treatment of patients with diabetic kidney disease (DKD).

According to cohort method, DKD patients were divided into control group and treatment group. The control group was given oral metformin tablets (0.5 g per time, twice a day), while treatment group was given oral dapagliflozin tablets (10 mg per time, once a day) on basis of control group. All patients were treated for 12 weeks. The clinical curative effect, glucose metabolism indexes [glycated hemoglobin (HbA1c), fasting blood glucose (FPG), 2 h postprandial blood glucose (2 h PG)], renal function [urine albumin/creatinine (UACR), serum creatinine (SCr), estimated glomerular filtration rate (eGFR)], renal vascular function [resistance index (RI), pulsatility index (PI), peak systolic velocity (PSV), end-diastolic velocity (EDV)], urine α-smooth muscle actin (SMA), membrane protein, transforming growth factor (TGF)-β1 and inflammatory factors [interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α] in the two groups were compared, and the safety was evaluated.

There were 40 cases in control group and 40 cases in treatment group. After treatment, difference in total response rate between treatment group and control group was statistically significant [92.50% (37 cases/40 cases) vs 72.50% (29 cases/40 cases), P<0.05]. After treatment, HbA1c levels in treatment group and control group were (6.52±0.76)% and (7.44±0.98)%; FPG levels were (7.11±1.05) and (8.05±1.21)mmol·L^-1; 2 h PG levels were (9.32±1.08) and (10.57±1.35) mmol·L^-1; UACR levels were (104.76±13.85) and (138.41±16.07)mg·g^-1; SCr levels were (82.27±10.38) and (101.68±13.54) μmol·L^-1; eGFR levels were (88.06±8.37) and (80.52±7.64) mL·min^-1·1.73 m^-2; RI levels were 0.51±0.10 and 0.65±0.13; PI were 1.15±0.24 and 1.49±0.31; PSV were (38.30±5.29) and (34.59±4.71) cm·s^-1; EDV were (15.73±2.49) and (13.41±2.02) cm·s^-1; levels of urine SMA were (26.31±2.39) and (30.47±2.86)kU·L^-1; levels of urine membrane protein were (528.41±50.78) and (581.65±57.22) μg·L^-1; levels of urine TGF-β1 were (85.01±9.82) and (102.94±13.57) μg·L^-1; levels of serum IL-1β were (26.93±3.36) and (40.14±4.57)ng·L^-1; levels of serum IL-6 were (14.36±1.59) and (17.94±2.01) ng·L^-1; levels of serum TNF-α were (30.22±3.37) and (43.81±4.06) ng·L^-1, and differences of all the above indexes between the two groups were statistically significant (all P<0.05). The adverse drug reactions were mainly on loss of appetite, diarrhea, fatigue and nausea in treatment group, while which were mainly on loss of appetite, headache and nausea in control group. There was no significant difference in total incidence of adverse drug reactions between treatment group and control group [12.50% (5 cases/40 cases) vs 7.50% (3 cases/40 cases), P>0.05].

Dapagliflozin combined with metformin can improve glucose metabolism, promote recovery of renal function and renal vascular function, regulate levels of SMA, membrane protein and TGF-β1, relieve inflammatory response and improve clinical curative effect in DKD patients.

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.