To evaluate the clinical efficacy and safety of siponimod tablets in patients with relapsing multiple sclerosis (RMS) through a case series study.

Patients meeting inclusion criteria from the department of neurology were enrolled. Demographic data, disease characteristics, medication history and laboratory/imaging results were collected. Efficacy was assessed at baseline, 3 months and 6 months after siponimod tablets medication using 3 dimensions: the expanded disability status scale (EDSS), patient-reported outcomes (PRO), and disease activity. Safety was concurrently evaluated.

A total of 7 patients were included. After 6 months of siponimod tablets treatment, median EDSS score decreased from 7.00 to 6.50; EQ-5D-5L utility index median increased from -0.06 to 0.20; EQ-5D-5L VAS median score rose from 52.86 to 63.57; MSIS-29v2 physical mean score decreased from 64.52 to 54.52; MSIS-29v2 psychological mean score declined from 51.85 to 44.44; MSWS-12 mean score reduced from 80.06 to 75.00. Magnetic resonance imaging (MRI) results indicated decreased disease activity, which was also observed in patients converting from teriflunomide to siponimod treatment. Adverse drug reactions including lymphopenia (2 cases), elevated transaminases (1 case) and hypertension (1 case) were all considered treatment-related.

Siponimod tablets may be a therapeutic option for RMS patients, though larger studies are needed to confirm efficacy. Pre-treatment assessment of complete blood count and liver function is essential. If clinically significant adverse drug reactions occur during the treatment period, adjustments to the dosage or combined medication should be considered.

To explore the the clincial efficacy and safety of butylphthalide soft capsules combined with dual anti-platelet therapy (DAPT) in the treatment of non-disabling ischemic cerebrovascular events (NICE).

The patients with NICE admitted to the hospital were enrolled as the research objects. According to random number table method, they were divided into treatment group and control group. Control group was treated with DAPT (aspirin enteric-coated tablets 100 mg·d^-1+ clopidogrel bisulfate tablets 75 mg·d^-1), while treatment group was treated with butylphthalide soft capsules 0.6 g·d^-1 on basis of control group for 1 month. The clinical curative effect, incidence of recurrent cerebral infarction within 6 months of follow-up, levels of NLR family Pyrin domain containing protein 3 (NLRP3) inflammasome, homocysteine (Hcy) and interleukin (IL)-6, plasma viscosity, whole blood high-shear viscosity, low-shear viscosity and hematocrit were compared between the two groups, and the safety was evaluated.

Among the 130 patients in this study, there were 120 cases included finally after excluding 10 cases not meeting the inclusion criteria. According to random number table method, they were divided into treatment group and control group, and there was no case lost to follow-up in the study process. After treatment, total response rate in treatment group was 93.33% (56 cases /60 cases) which was statistically significantly higher than that in control group [80.00% (48 cases /60 cases), P<0.05]. After treatment, scores of National Institutes of Health stroke scale (NIHSS) in treatment group and control group were (1.10±0.12) and (1.85±0.21) points, scores of modified Rankin scale (mRS) were (1.10±0.12) and (1.82±0.19) points, scores of activity of daily living (ADL) were (68.97±6.96) and (60.11±6.12) points, levels of NLRP3 inflammasome were (1.40±0.16) and (1.96±0.21) μg·L^-1, IL-6 levels were (24.15±2.57) and (31.27±3.35) pg·mL^-1, Hcy levels were (20.18±2.13) and (27.78±3.14) μmol·L^-1, plasma viscosity were (1.59±0.16) and (1.81±0.19) mPa·s^-1, whole blood high-shear viscosity were (4.01±0.41) and (4.78±0.50) mPa·s^-1, whole blood low-shear viscosity were (10.42±1.15) and (11.87±1.20) mPa·s^-1, and hematocrit were (0.25±0.03) and (0.33±0.04) L·L^-1, there were statistically significant differences in the above indexes between the two groups (all P<0.05). After 6 months of follow-up, incidence of recurrent cerebral infarction in treatment group was 8.33% (5 cases /60 cases) which was statistically significantly lower than that in control group [23.33% (14 cases / 60 cases), P<0.05]. The main adverse drug reactions in treatment group were subcutaneous ecchymosis 1 case (1.67%), nausea 1 case (1.67%) and gastrointestinal discomfort 3 cases (5.00%), while which in control group were subcutaneous ecchymosis 2 cases (3.33%), nausea 2 cases (3.33%), vomiting 1 case (1.67%) and gastrointestinal discomfort 2 cases (3.33%). There was no significant difference in total incidence of adverse drug reactions between treatment group and control group (8.33% vs 11.67%, P>0.05).

Curative effect of butylphthalide soft capsule combined with DAPT is good in NICE patients, which can reduce level of NLRP3 inflammasome, improve blood circulation, reduce incidence of recurrent cerebral infarction and will not increase adverse drug reactions.

To investigate the efficacy and safety of oliceridine injection, a novel G protein-biased μ-opioid receptor agonist, compared with sufentanil injection, a traditional μ-opioid receptor agonist, during the perioperative period of proximal femoral nail antirotation (PFNA) internal fixation in elderly patients with intertrochanteric femoral fractures.

A toal of 80 elderly patients with intertrochanteric femoral fractures scheduled for PFNA internal fixation from April 2024 to April 2025 were randomly divided into control group and treatment group. In the control group, sufentanil injection 0.3 μg·kg^-1 was used for intraoperative induction, and patient-controlled intravenous analgesia (PCIA) after surgery consisted of sufentanil injection 1 μg·kg^-1 plus flurbiprofen axetil injection 200 mg. In the treatment group, oliceridine injection 0.06 mg·kg^-1 was used for intraoperative induction, and postoperative PCIA consisted of oliceridine injection 0.2 mg·kg^-1 plus flurbiprofen axetil injection 200 mg. The time to first ambulation after surgery,15-item Quality of Recovery Scale (QoR-15) scores at 24 and 48 h after surgery, intraoperative hemodynamic changes, visual analogue scale (VAS) scores at 6, 12, 24 and 48 h after surgery and adverse drug reactions were compared between two groups.

Forty patients were enrolled in each group. For the primary outcome measures, the QoR-15 scores at 24 hours after surgery (T7) in the treatment group and the control group were (123.23±8.82) and (114.80±10.55) scores, respectively; the QoR-15 scores at 48 hours after surgery (T8) were (126.65±6.13) and (118.20±9.13) scores, respectively; the time to first ambulation after surgery were (43.53±4.44) and (46.83±4.13) hours, respectively. The differencs of above indexes between two groups were all statistically significant (all P<0.05). For the secondary outcome measures, no statistically significant differences were found between the two groups in intraoperative hemodynamic parameters or postoperative VAS pain scores within 48 hours after surgery (all P>0.05). The incidence of postoperative dizziness in the treatment group and control group was 7.50% (3 cases/40 cases) and 27.50% (11 cases/40 cases), respectively; the incidence of postoperative nausea and vomiting was 7.50% (3 cases/40 cases) and 25.00% (10 cases/40 cases), respectively; the incidence of postoperative constipation was 5.00% (2 cases/40 cases) and 20.00% (8 cases/40 cases), respectively; statistically significant differences were noted in the incidences of the above adverse reactions between the two groups (all P<0.05). However, the incidence of postoperative cognitive dysfunction was 2.50% (1 cases/40 cases) and 7.50% (3 cases/40 cases), respectively, with no statistically significant difference (P>0.05).

In elderly patients undergoing PFNA internal fixation, oliceridine injection provides intraoperative hemodynamic stability and postoperative analgesic efficacy comparable to sufentanil injection. Moreover, it significantly reduces the incidence of opioid-related adverse reactions such as dizziness, nausea and vomiting, and constipation, shortens the time to first ambulation, improves the early postoperative quality of recovery, and facilitates enhanced recovery after surgery.

To observe the clinical efficacy and safety of 2 chemotherapy regimens in the treatment of metastatic breast carcinoma with overexpression of human epidermal growth factor receptor 2 (HER2): one was the dual-targeted therapy with herceptin injection + pertuzumab injection (herceptin + pertuzumab, HP) combined with paclitaxel injection (albumin-bound) + carboplatin injection, and the other was HP dual-targeted therapy combined with paclitaxel injection alone.

Patients were divided into control group and treatment group based on the treatment regimen. Control group received HP dual-targeted therapy (herceptin for injection: initial dose of 8 mg·kg^-1, followed by 6 mg·kg^-1; pertuzumab injection: initial dose of 840 mg, followed by 420 mg) combined with paclitaxel injection (125 mg·m^-2) for chemotherapy. Treatment group additionally received carboplatin injection with an area under the curve (AUC) of 6 on the basis of the treatment regimen of control group, with 21 days as one cycle, for a total of 6 cycles. The clinical efficacy, levels of tumor markers, survival benefits of the 2 groups were compared, and safety evaluation was also conducted.

The control and treatment groups comprised 52 and 54 subjects, respectively. After treatment, the objective response rates of the treatment group and the control group were 74.07% (40 cases/54 cases) and 53.85% (28 cases/52 cases), respectively, the carbohydrate antigen 15-3 (CA153) levels were (21.82±3.22) and (23.56±3.43) U·mL^-1, respectively; the carcinoembryonic antigen (CEA) were (2.22±0.53) and (2.51±0.63) μg·L^-1, respectively; the levels of vascular endothelial growth factor A (VEGFA) were (53.51±7.44) and (57.43±8.04) ng·mL^-1, respectively; trefoil factor 1 (TFF1) were (1.51±0.43) and (1.74±0.59) mg·L^-1, respectively; there were significant differences in the above indexes between experimental group and control group (all P<0.05); the positive rates of anti-drug antibody (ADA) were 3.85% and 1.85%, respectively and the positive rates of neutralizing antibody (NAB) were 1.92% and 1.85% respectively, without statistically significant differences (all P>0.05). The median progression free survival (PFS) of treatment group was 14.5 months, which was significantly higher than that of control group (11.3 months); the median overall survival (OS) of treatment group was 30.0 months, which was significantly higher than 25.4 months of control group (all P<0.05). Survival advantage was observed in treatment group (75.93%) compared to control group (57.69%), win statistically significant difference (P<0.05). During treatment, 34 patients (62.96%) in treatment group experienced alopecia, 25 (46.30%) had nausea and 19 (35.19%) had vomiting; in control group, 43 patients (82.69%) had alopecia, 11 patients (21.15%) had nausea, and 8 patients (15.38%) had vomiting. Compared with control group, treatment group had statistically significantly higher incidence of nausea and vomiting, and statistically significantly lower incidence of alopecia (all P<0.05).

Compared with the regimen of HP dual-targeted therapy combined with paclitaxel injection alone, the regimen of HP dual-targeted therapy combined with paclitaxel injection + carboplatin injection can more effectively reduce the levels of tumor markers in patients with HER2-positive metastatic breast cancer, improve the short-term and long-term efficacy and prognosis of patients, and the two regimens have similar serum immunogenic characteristics.

To observe the clinical efficacy of roxadustat capsules combined with levocarnitine injection in patients with renal failure undergoing combined hemoperfusion (HP) and hemodialysis (HD).

Patients with chronic renal failure were randomly divided into control group and treatment group using a random number table method. The control group was treated with HP+HD combined with intravenous levocarnitine (1.0 g per session, 3 times per week). On the basis of control group, treatment group received additional oral roxadustat capsules. The starting dose was selected according to the patient’s body weight: 100 mg per dose (45-60 kg) or 120 mg per dose (≥60 kg), 3 times per week, with dose adjustments made every 4 weeks. The total course of treatment was 12 weeks. The renal function parameters, nutritional status indicators, iron metabolism-related indices, medical research council (MRC) scores and clinical efficacy were compared between the two groups, and the safety was assessed.

A total of 165 patients who met the preliminary screening criteria were screened for this study. According to the inclusion and exclusion criteria, 17 ineligible patients were excluded, resulting in 148 patients being ultimately enrolled. These participants were randomly assigned to either the treatment group or the control group, with 74 patients in each. No dropouts occurred in either group during the trial. After treatment, the levels of serum creatinine (Scr) in the control group and the treatment group were (338.46±35.69) and (321.94±49.87) mL·min^-1, respectively; the albumin (ALB) levels were (35.74±5.32) and (38.12±6.07) g·L^-1, respectively; the hemoglobin (HB) levels were (112.26±11.79) and (118.17±8.16) g·L^-1, respectively; the HB compliance rates were 60.81% and 82.43%, respectively; the serum iron (SI) levels were (13.85±2.87) and (15.34±2.93) μmol·L^-1, respectively; the serum ferritin (SF) levels were (328.87±54.36) and (351.87±42.74) ng·mL^-1, respectively; the transferrin saturation (TSAT) levels were (28.97±6.29)% and (32.17±6.75)%, respectively; and the MRC total scores were (49.20±8.77) and (53.26±6.91) points, respectively. The treatment group demonstrated statistically significantly greater improvement in the aforementioned indices compared to control group (P<0.05, P<0.01). The main adverse drug reactions of treatment group were nausea and vomiting, elevated blood pressure, muscle spasm and diarrhea; the control group had nausea and vomiting, elevated blood pressure, headache, muscle spasm and diarrhea. The total incidence of adverse drug reactions in treatment group and control group were 9.46% and 12.16%, respectively, with no statistically significant difference (P>0.05).

The combination of roxadustat capsules and levocarnitine injection effectively reduces renal impairment, improves nutritional and iron status, alleviates muscle weakness, and is well-tolerated in chronic renal failure patients undergoing combined HP+HD therapy.

To observe the efficaly and safety of combination regimen of anlotinib with pemetrexed and carboplatin in patients with advanced lung adenocarcinoma with acquired resistance to tyrosine kinase inhibitor (TKI).

Patients with advanced lung adenocarcinoma with acquired TKI resistance were divided into control group and treatment group according to the treatment methods. Patients in the control group received intravenous infusions of pemetrexed disodium for injection (500 mg·m^-2) and carboplatin injection (dose cauculated based on area under the blood concentration-time curve 6 g·L^-1·min^-1) on the first day of each treatment cycle, with each 3 weeks as one cycle. On the basis of the control group, the treatment group was given anlotinib hydrochloride capsules, which were taken 10 mg orally continuously for 2 weeks starting from day 1 of each cycle, followed by a 1-week drug holiday. Each 3-week period constituted one treatment cycle. Both groups were continuously treated for 4 cycles or more. The therapeutic outcomes, tumor marker concentrations, and vascular endothelial growth factor (VEGF) levels, immune function, safety evaluation, and long-term efficacy were compared between the two groups.

A total of 102 cases were enrolled; there were 48 cases in control group and 54 cases in treatment group. Disease control rate of control group and treatment group were 64.58% (31 cases/48 cases) and 83.33% (45 cases/54 cases), respectively; the carbohydrate antigen 125 levels were (52.38±7.21) and (48.49±6.12) U·mL^-1, respectively; the carcinoembryonic antigen levels were (8.29±1.79) and (7.52±1.21) μg·L^-1, respectively; the neuron-specific enolase levels were (26.17±4.33) and (23.84±3.32) μg·L^-1, respectively; the VEGF-A levels were (95.38±10.76) and (89.47±11.32) pg·mL^-1, respectively; the VEGF-B levels were (87.41±9.76) and (82.63±8.13) pg·mL^-1, respectively; and the VEGF-C levels were (61.56±7.49) and (58.67±6.20) pg·mL^-1, respectively. Comparison of all measured parameters in the treatment group and control group demonstrated statistically significant differences (all P<0.05). Adverse event rate of control group and treatment group were 37.50% (18 cases/48 cases) and 42.59% (23 cases/54 cases) respectively; median progression-free survival were 16 and 21 months, respectively; overall survival were 22 and 34 months, respectively; compared between 2 groups, the differences of the above indicators were not statistically significant (all P>0.05).

The addition of anlotinib to pemetrexed and carboplatin in patients with TKI-acquired resistant advanced lung adenocarcinoma significantly enhances the efficacy and immunomodulation, and inhibits the tumor growth at the same time, with a good safety profile and long-term efficacy.

To observe clinical curative effect and safety of intravenous drip and aerosol inhalation of colistimethate sodium for injection in patients with severe neurological disease and Acinetobacter baumannii (AB) pulmonary infection.

According to queuing method, patients with severe neurological disease and AB pulmonary infection in the hospital were divided into treatment group and control group. Control group was treated with colistimethate sodium for injection (150 mg bid, intravenous drip), while treatment group was treated with colistimethate sodium for injection (75 mg bid, aerosol inhalation) on basis of control group. All patients were treated for 5 days. The clinical curative effect, renal function, inflammatory response, bacterial clearance rates and prognosis in the two groups were compared, and the safety was evaluated.

Among the 80 patients, there were 40 cases in treatment group and 40 cases in control group. After treatment, total response rates of treatment group and control group were 72.50% (29 cases/40 cases) and 42.50% (17 cases/40 cases), levels of serum interleukin-8 were (4.07±1.01) and (5.01±1.65) pg·mL^-1, procalcitonin levels were 0.90(0.60, 1.35) and 1.50(1.05, 2.00) ng·mL^-1, C-reactive protein levels were (5.57±3.28) and (10.57±6.09) mg·L^-1, bacterial clearance rates were 60.00% (24 cases/40 cases) and 35.00% (14 cases/40 cases), and infection-related 28 d mortality rates were 5.00% (2 cases/40 cases) and 20.00% (8 cases/40 cases), the differences between the two groups were all statistically significant (all P<0.05). After treatment, levels of serum creatinine in treatment group and control group were (86.22±9.84) and (87.27±10.54) μmol·L^-1, and levels of blood urea nitrogen were (7.98±2.44) and (7.86±2.47) mmol·L^-1, the differences were not statistically significant (both P>0.05). The main adverse drug reactions in treatment group were rash, diarrhea and respiratory depression, while which in control group were rash and diarrhea. The difference in total incidence of adverse drug reactions between treatment group and control group was statistically significant (7.50% vs 5.00%, P>0.05).

Curative effect of intravenous drip combined with aerosol inhalation of polymyxin E is significant in patients with severe neurological disease and AB infection, which can effectively increase bacterial clearance rate, reduce inflammatory response and mortality, and will not increase renal injury.

To investigate the effect of L-carnitine on hypoxic-ischemic brain damage in neonatal mice by regulating PI3K/AKT pathway.

Eighty mice with successful hypoxic-ischemic brain damage models were randomly divided into model group, L-carnitine low-dose group, L-carnitine medium-dose group and L-carnitine high-dose group, with 20 mice in each group, and 20 mice without modeling were used as sham operation group. The mice in the L-carnitine low-dose group, L-carnitine medium-dose group and L-carnitine high-dose group were intraperitoneally injected with L-carnitine at 100, 250 and 500 mg·kg^-1, respectively. The mice in the sham-operation group and the model group were intraperitoneally injected with the same amount of normal saline, the administration lasted for one week. The pathological changes of brain tissue were analyzed by hematoxylin-eosin staining. TCC staining was used to analyze the cerebral infarction area. The apoptosis of neurons in mouse brain tissue was analyzed by in situ terminal assay. The levels of inflammatory factors in brain tissue of mice were detected by enzyme-linked immunosorbent assay. The expression levels of PI3K/AKT pathway-related proteins were detected by Western blotting.

The brain tissue cells of the sham operation group were closely arranged and the structure was intact. In the model group, the brain tissue structure was disordered, a large number of cells were shed, the intercellular space was enlarged, and the morphology was swollen. The brain tissue loss of mice in different L-carnitine dose groups was gradually improved. The cerebral infarction rates in the sham-operated group, the model group, the low-dose L-carnitine group, the middle-dose L-carnitine group, and the high-dose L-carnitine group were (0.83±0.08)%, (59.32±3.12)%, (33.72±1.55)%, (25.58±1.21)%, and (9.81±1.07)%, respectively; the apoptosis rates of neurons were (1.85±0.18)%, (37.31±1.25)%, (21.67±1.02)%, (15.62±2.31)% and (6.63±0.88)%, respectively; the levels of interleukin-6 were (1.32±0.08), (13.21±1.16), (9.33±0.19), (6.03±0.18) and (3.73±0.15) pg·mL^-1, respectively; the levels of tumor necrosis factor α were (2.02±0.15), (15.07±1.26), (10.08±2.06), (7.13±1.16) and (4.06±0.08) pg·mL^-1, respectively; the relative expression levels of PI3K protein were 0.65±0.09, 0.10±0.01, 0.19±0.03, 0.35±0.03 and 0.55±0.06, respectively; the relative AKT protein expression levels were 0.69±0.05, 0.11±0.02, 0.21±0.02, 0.39±0.03 and 0.63±0.06, respectively. Compared with the model group, the above indicators in the L-carnitine low-dose group, the L-carnitine medium-dose group and the L-carnitine high-dose group had statistically significant differences (all P<0.05).

L-carnitine can alleviate hypoxic-ischemic brain damage in neonatal mice, and its mechanism may be related to the regulation of PI3K/AKT signaling pathway.

To observe clinical efficacy and safety of low-dose sitagliptin tablets combined with dapagliflozin tablets in the treatment of elderly patients with diabetic kidney disease (DKD).

According to random number table method, elderly patients with DKD admitted to the hospital were divided into group A (low-dose sitagliptin tables, 50 mg qd), group B (dapagliflozin tables, 10 mg qd) and group C (low-dose sitagliptin tables, 50 mg qd combined with dapagliflozin tables,10 mg qd). All patients were treated for 3 months. The clinical curative effect and changes in fasting blood glucose (FBG), 2 h postprandial blood glucose (2 h PG), glycosylated hemoglobin (HbA1c), estimated glomerular filtration rate (eGFR), serum creatinine (SCr), blood urea nitrogen (BUN), uric acid (UA), monocyte chemoattractant protein-1 (MCP-1), adiponectin (APN), nuclear factor-κB (NF-κB) and urinary albumin creatinine ratio (UACR) were compared among the three groups, and the safety evaluation was performed.

In this study, there was no shedding cases. Among the 129 patients, there were 43 cases in group A, 43 cases in group B and 43 cases in group C. After treatment, response rate of group C was 95.35% (41 cases /43 cases), which was significantly higher than that of group A [79.07% (34 cases /43 cases)] and group B [81.40% (35/43 cases)] (all P<0.05). After treatment, HbA1c levels in group A, group B and group C were (7.17±1.21)%, (6.64±1.06)% and (6.13±1.14)%; SCr levels were (94.37±12.16), (86.19±11.45) and (80.45±10.37) μmol·L^-1; and UACR were (80.04±8.36), (71.19±7.72) and (53.04±6.81) mg·g^-1, respectively. Compared with group A, the above indexes were statistically significantly decreased in group B and group C, and which were statistically significantly lower in group C than group B (all P<0.05). After treatment, eGFR in group A, group B and group C were (81.50±9.12), (92.41±9.56) and (103.73±10.24) mL·min^-1 · 1.73 m^-2, respectively. Compared with group A, eGFR was statistically significantly increased in group B and group C, and which was statistically significantly higher in group C than group B (P<0.05). After treatment, MCP-1 levels in group A, group B and group C were (85.38±8.42), (91.40±9.28) and (73.12±8.06) pg·mL^-1; NF-κB levels were (4.09±1.08), (4.71±1.22) and (3.52±0.85) ng·mL^-1, respectively. Compared with group B, the above indexes were statistically significantly decreased in group A and group C, and which were statistically significantly lower in group C than group A (both P<0.05). After treatment, APN levels in group A, group B and group C were (10.17±2.06), (9.15±1.50) and (11.24±2.17) pg·mL^-1, respectively. Compared with group B, APN was statistically significantly increased in group A and group C, and which was statistically significantly higher in group C than group A (P<0.05). The main adverse drug reactions in group A were gastrointestinal discomfort and nasopharyngitis; in group B were gastrointestinal discomfort, hypotension and urinary and reproductive system infection, and in group C were hypoglycemia and gastrointestinal discomfort. There was no significant difference in total incidence of adverse drug reactions among group A, group B and group C (30.23% vs. 20.93% vs. 27.91%, all P>0.05). Pearson correlation analysis showed that decrease of UACR after treatment was positively correlated with the decrease of NF-Κb and MCP-1 and the increase of APN (r=0.419, 0.524, 0.485, all P<0.05).

There is a synergistic effect of low-dose sitagliptin combined with dapagliflozin in the treatment of elderly patients with DKD, which can significantly improve blood glucose metabolism indexes, enhance renal function, regulate levels of inflammatory factors and effectively reduce UACR, with good safety.

To investigate the temporal association and molecular mechanism of bortezomib-induced mitochondrial oxidative stress and apoptosis in Schwann cells.

Rat Schwann RSC96 cells were cultured in vitro and treated with different concentrations of bortezomib to establish an in vitro model of bortezomib damaged RSC96 cells. The assessment of cell viability was conducted by means of the CCK-8 method, and the morphological alterations observed in each group of cells were documented through inverted microscope analysis. DCFH-DA and Hoechst staining were combined with fluorescence microscopy to determine the content of reactive oxygen species. JC-1 staining was used to detect mitochondrial membrane potential level, and the degree of mitochondrial permeability transition pore opening and Ca²⁺ concentration were detected by fluorescence microscope. Annexin V-FITC/PI dual labeling was used to detect cell apoptosis. ELISA was used to detect the levels of inflammatory factors TNF-α, IL-1β, and IL-6.

In comparison with the control group, as the bortezomib concentration increased, the viability of RSC96 cells decreased in a concentration-dependent manner. The cell gap increased, the number of cells decreased significantly, the nucleus solidified, and the cells exhibited typical characteristics of apoptosis. Furthermore, bortezomib induced a reactive oxygen species burst in RSC96 cells in a dose-dependent manner, resulting in depolarization of mitochondrial membrane potential, cytosolic Ca²⁺ overload, continuous opening of the mitochondrial permeability transition pore, and a significant increase in the apoptosis rate of RSC96 cells.

Bortezomib has been shown to induce programmed cell death apoptosis in Schwann cells by activating an axis involving oxidative stress, mitochondrial damage, and subsequent apoptosis. This finding suggests that oxidative stress and mitochondrial damage may represent pivotal mechanisms of bortezomib-induced toxicity, thus providing a novel target for the intervention of BIPN.