Sepsis-associated encephalopathy (SAE), the most prevalent and severe complication of sepsis, is a leading cause of long-term cognitive deficits and increased mortality. Although anti-inflammatory and antioxidant therapies have advanced, single-target drugs cannot disrupt the complex inflammatory cascade in SAE. Therefore, multi-target synergistic strategies are urgently needed. This study developed a multifunctional biomimetic nanodrug, ME@FDsi, for precise SAE therapy. The system uses a tetrahedral framework nucleic acid (tFNA) as a carrier, connected via base complementary pairing with small interfering RNA (siTNFα) to target TNF-α. It is also loaded with disulfiram (DSF) to inhibit pyroptosis. The resulting FDsi was encapsulated in erythrocyte membrane vesicles modified with the M1 microglia-targeting MG1 peptide. ME@FDsi exhibits a nanovesicle structure, prolonged circulation, stability, and biocompatibility. In SAE mice, it crosses the compromised blood-brain barrier and targets M1 microglia via MG1, releasing DSF and siTNF-α intracellularly. DSF blocks pyroptosis and IL-1β release, while siTNFα silences TNF-α expression. Additionally, tFNA scavenges reactive oxygen species. Together, these actions shift microglia from the M1 to the M2 phenotype. ME@FDsi treatment improved cognitive function, reduced multi-organ damage, and increased survival in SAE mice. This multi-mechanism synergistic approach offers a promising therapeutic strategy for clinical SAE and sepsis.

BACKGROUND Endoscopic gastrointestinal surgery rarely leads to airway compromise, but when mediastinal emphysema or pneumoperitoneum caused by perforation occurs, it can result in acute respiratory failure under anesthesia. Since the underlying mechanisms differ from those of typical pulmonary causes, reporting such rare cases is valuable for raising awareness among anesthesiologists and clinicians, and for emphasizing the importance of understanding surgical progress and performing timely physical examinations. CASE REPORT A 60-year-old woman with a submucosal esophageal mass underwent submucosal tunnel endoscopic resection (STER). During the procedure, a critical event occurred: airway pressure surged and effective ventilation nearly ceased, manifesting as hypoxemia and hypotension. Physical examination revealed marked abdominal distension with elevated intra-abdominal pressure. Concurrent intraoperative observation identified a perforation in the lower esophagus. The diagnosis was an esophageal perforation leading to pneumoperitoneum-induced abdominal compartment syndrome, which caused thoracic compression and acute respiratory failure. Emergency management included halting the procedure and CO₂ insufflation, followed by immediate abdominal decompression. These interventions promptly restored adequate ventilation and stabilized hemodynamics. CONCLUSIONS Esophageal perforation during lower esophageal tumor dissection can permit gas to escape into the abdominal cavity, leading to abdominal compartment syndrome and subsequent thoracic compression. This cascade can rapidly progress to severe hypoventilation and hypoxemia. Awareness of this rare but potentially fatal complication is crucial, and timely recognition with prompt management is essential to improving patient safety during gastrointestinal surgery.

BACKGROUND The interspace between the popliteal artery and posterior capsule of the knee block (IPACK) combined with adductor canal block (ACB) has short-term analgesic effect after arthroscopic knee surgery(AKS), and prolonging the duration of analgesia is very important for patients to recover quickly after surgery. The purpose of this study was to investigate whether perineural dexmedetomidine (DEX) or intravenous can prolong the analgesic time of IPACK and ACB, and ultimately promote the postoperative rehabilitation of patients undergoing AKS. MATERIAL AND METHODS In this randomized controlled trial, 102 eligible AKS patients were allocated to 3 groups: perineural DEX with ropivacaine for Group E (n=34), intravenous DEX for Group I (n=34), and standard IPACK-ACB (ropivacaine alone) for Group C (n=34). The outcomes included resting and active Visual Analog Scale (VAS) scores at 6 h, 12 h, 24 h, 48 h, 54 h, and 60 h postoperatively, inflammatory marker levels on the first postoperative day, and maximum walking distance at 24 and 48 hours after surgery. RESULTS There were no significant demographic differences between the 3 groups. Resting and active VAS scores in Group E were significantly lower than those in Group C within 48 hours postoperatively (P<0.05), VAS at 48 h resting state (P<0.001, mean difference,-1.15; 95% CI, -1.65 to -0.65), VAS at 48 h active state (P<0.001, mean difference,-0.91; 95% CI, -1.32 to -0.50). On the first postoperative day, IL-1β levels in Groups E and I were significantly lower than in Group C (P<0.05). Group E had a significantly longer maximum walking distance at 24 and 48 hours after surgery compared to Groups I and C (P<0.001). CONCLUSIONS Perineural DEX prolongs IPACK-ACB analgesia to 48 hours, improves functional recovery, and attenuates IL-1β release, outperforming intravenous administration. These findings support the integration of route-specific DEX into enhanced recovery protocols for AKS.

Anti-inflammatory and antioxidant regimens are routine strategies for the treatment of various inflammatory diseases; however, existing clinical therapies are usually ineffective. Here, we demonstrate a broad-spectrum anti-inflammatory combined antioxidant strategy based on self-derived polymorphonuclear neutrophils (PMNs) and a novel "cryo-death" technology, which can be widely applied to diverse inflammatory diseases. Through TNF-alpha pre-activation, buffering at-80 degrees C for 20 min, immersion in liquid nitrogen, and loading with catalase, engineered cryo-dead PMNs (Cat@P-CD-PMNs) were created from live PMNs, which eliminated intrinsic inflammation-causing effects while retained intact cellular structure, functional receptors (e.g., proinflammatory cytokine receptors, adhesion molecules, and chemokine receptor), and inflammation- recruitment capacity. In a mouse model of sepsis, intravenously injected Cat@P-CD-PMNs rapidly (within 1 h) and precisely migrated to inflammatory damaged organs, meanwhile utilizing multiple pro-inflammatory cytokine receptors expressed on their surface and targeted delivered catalase for broad-spectrum neutralization of pro-inflammatory cytokines and efficient scavenging of reactive oxygen species, respectively. After treatment, the mice's body temperature was recovered, the inflammatory injuries were dramatically alleviated, and the mortality rate was reduced from 100 % to 25 %. More importantly, Cat@P-CD-PMNs fabricated from PMNs of septic patients were able to effectively eliminate a variety of pro-inflammatory cytokines in their own plasma. In murine models of COVID-19 and skin wounds, Cat@P-CD-PMNs were administrated via inhalation and spraying, respectively, and showed long-term residency (over 96 h) in the inflammatory damaged tissues. Meanwhile, Cat@P-CD-PMNs exhibited obvious anti-inflammatory and antioxidant effects, which notably prolonged survival time of COVID-19 mice (from 6 to 10 days) and promoted rapid wound healing, respectively. Such autologous dead cells avoid the potential risk of immune rejection and can be phagocytosed and cleared by macrophages, presenting tremendous prospects for clinical translation.

BACKGROUND Arthroscopic knee surgery (AKS) is minimally invasive, reducing hospital stay compared to traditional surgery, but postoperative pain remains a significant issue. This study compared the analgesic and functional outcomes following AKS following anesthesia using adductor canal block (ACB) with and without anesthesia using the interspace between the popliteal artery and posterior capsule of the knee (IPACK) block under spinal anesthesia (SA). MATERIAL AND METHODS We randomly allocated 120 patients into 3 groups: IPACK+ACB+SA for Group A (n=40), ACB+SA for Group B (n=40), and SA for Group C (n=40). The outcome was the visual analog scale (VAS) score evaluated at rest and during activity at 3 h, 6 h, 12 h, 24 h, and 48 h postoperatively, the frequency of administration of postoperative rescue analgesic, and the maximal walking distance at 24 h and 48 h postoperatively. RESULTS Compared with Group C, the VAS scores in Group A were significantly lower at 48 h postoperatively (P<0.05). There was a significant difference in the frequency of postoperative rescue analgesia use among the 3 groups (P=0.001). In a subgroup analysis of meniscus shaping under arthroscopy, the resting VAS score in Group A was lower than that in Group B and Group C at 48 h postoperatively (P<0.05). The maximum walking distance of Group A was longer than that of Group B and Group C at 24 h and 48 h postoperatively (P<0.01). CONCLUSIONS The effect of postoperative analgesia in the group receiving IPACK combined with ACB after AKS was obviously superior. In arthroscopic meniscus repair surgery, the duration of analgesia was longer, and the maximum walking distance at 48 h postoperatively was longer.

Utilizing drug-loaded hydrogels to restore nerve conductivity emerges as a promising strategy in the treatment of spinal cord injury (SCI). However, many of these hydrogels fail to deliver drugs on demand according to the dynamic SCI pathological features, resulting in poor functional recovery. Inspired by the post-SCI microenvironments, here we report a time-sequential and controllable drug delivery strategy using an injectable hydrogel responsive to reactive oxygen species (ROS) and matrix metalloproteinases (MMPs). This strategy includes two steps: first, the hydrogel responds to ROS and releases nanodrugs to scavenge ROS, thereby mitigating inflammation and protecting neurons from oxidative stress in the initial SCI stages; second, the accumulation of MMPs triggers the release of vascular endothelial growth factor from nanodrugs to promote angiogenesis and neural stem cell differentiation in the late stage of SCI. In two clinically relevant SCI models, a single injection of the hydrogel led to an efficient structural and functional recovery of SCI 6 weeks after the intervention. We observed less inflammation, fibrosis, and cavities but more angiogenesis and neurons in the hydrogel-treated injured spinal cord region compared with the untreated animals. The hydrogel exhibits mechanical strength and conductivity comparable to natural spinal cord, facilitating its further clinical translation.

BACKGROUND Hyperparathyroidism is a common issue in patients on long-term hemodialysis, necessitating parathyroidectomy with deep venipuncture. These patients frequently exhibit a heightened incidence of vascular calcification, complicating deep venipuncture and increasing the risk of associated complications. Therefore, a crucial aspect of preoperative assessment in this population involves identifying vascular calcification, with a preference for ultrasound-guided intraplane puncture. Special care is required to prevent blood vessel injuries and postoperative complications such as deep vein thrombosis. CASE REPORT We present the case of a 66-year-old woman with secondary hyperparathyroidism who encountered challenges during an internal jugular vein puncture, leading to subsequent thrombosis. Initial attempts were hindered by calcification of the internal jugular vein's vascular wall, resulting in stratified damage to the vessel's wall. However, the ultrasound-guided in-plane puncture technique successfully allowed the insertion of a central venous catheter without further damage to the vascular wall. On the postoperative fourth day, thrombus formation was observed in the damaged vascular wall from the initial puncture. CONCLUSIONS The ultrasound-guided in-plane puncture technique is advantageous in overcoming the difficulties associated with puncturing through deep vein calcification in patients with secondary hyperparathyroidism. This technique also diminishes the likelihood of complications such as venous thrombosis.

This prospective randomized trial was conducted to compare the quality and outcome of perioperative anesthesia between axillary brachial plexus block combined with axillary nerve block (axillary approach group,AX) and supraclavicular brachial plexus block( supraclavicular block group, SU). The primary outcome measure was to compare anesthesia quality evaluation including sensory function, motor function, and subjective feeling scores during skin incision, 30 minutes after skin incision, and at the end of surgery, and postoperative analgesia maintenance time score. Secondary outcomes included the number of patients in whom sufentanil was used, dexmedetomidine (Dex) dose, duration of sensory and motor blocks, number of patients who required remedial analgesia, and procedural complications.The proportion of patients in whom good-to-excellent anesthesia quality was achieved in AX group and SU group were 80% and 76.7%, respectively; anesthesia failure did not occur in both groups. Both procedures met the needs of surgical anesthesia and analgesia. Anesthesia quality and incidence of sufentanil use did not significantly differ between the groups. The incidence of phrenic nerve palsy was significantly higher in the supraclavicular block group (30% vs. zero; P = 0.002).Ultrasound-guided axillary brachial plexus block combined with axillary nerve block can achieve similar anesthesia quality and outcome as supraclavicular brachial plexus block,and found to have similar success rates. Trial registratio: http://www.chictr.org.cn with the registration number of ChiCTR2200057906. Date of first trial of 21/03/2022.

Transversus abdominis plane block is an anesthesia method that injects local anesthetics into the abdominal muscle fascia to produce analgesic effects. It is widely used in abdominal surgery and in pain management. This expert consensus introduces the relevant anatomy, and systematically describes the various techniques, common drugs, indications, contraindications and complications of transversus abdominis plane block, to guide the application of this method in the clinic.

Nerve block is an important part of postoperative multimodal analgesia. Rectus sheath block is one of the commonly used nerve block methods in clinical practice, which mainly blocks the anterior cutaneous branch of intercostal nerves. This method has a clear analgesic effect on midline abdominal incision, and has a good application in pain diagnosis and treatment. This expert consensus introduces the related anatomical structure, blocking method, commonly used drugs, complications and clinical application of rectus sheath block in order to guide the clinical practice.

Paclitaxel is an extensively used chemotherapy antitumor drug and paclitaxel-induced peripheral neuropathy (PIPN) is one of the most common side effect. Rapamycin, originally used as an adjuvant drug for chemotherapy, has recently been found to possess potential neuroprotective activities. Our purposes of this study are to verify the effect of rapamycin on PIPN, which contributes to a new target for PIPN treatment. Mice were given paclitaxel or rapamycin with different injection methods. Paw withdrawal threshold was tested at different time points for mechanical sensitivity assessment. Administration of paclitaxel, both 2 mg/kg and 5 mg/kg, could induce mechanical hypersensitivity. 0.01 mg intrathecal injection of rapamycin showed the best effect on attenuate the mechanical hyperalgesia of PIPN. Intrathecal injection of only rapamycin would not induce the mechanical hyperalgesia while when rapamycin and paclitaxel were used together the mechanical hyperalgesia induced by paclitaxel could be attenuated. Paclitaxel could induce mechanical hyperalgesia in mice and rapamycin could attenuate such mechanical hyperalgesia of PIPN.

Liberal oxygen therapy (LOT) is widely used as adjuvant therapy in the treatment of critically ill patients. However, excessive medical intervention in the treatment of high-concentration hyperoxia can destroy the physiological balance of the body and even lead to serious complications. Reducing iatrogenic complications and mortality is a new demand in recent years to further improve health levels and cure rates. This paper analyzes the relevant research in recent years, and expounds on the clinical role of conservative oxygen therapy (COT) and its relationship with the near and long-term complications and mortality of related diseases, to provide a clinical and theoretical basis for improving the effect of oxygen therapy and reducing the related complications.

Objective:To observe the effect of nalbuphine and parecoxib therapy attenuates remifentanil-induced hyperalgesia (RIH) after surgery.Methods:A total of 100 patients who were scheduled for laparoscopic hysterectomy were selected. According to the random number table method, they were divided into four groups: a sufentanil group (group S, n=23), which was administered with 0.30 μg/kg sufentanil during anesthesia induction followed by intermittent addition of sufentanil during surgery for anesthesia maintenance; a remifentanil group (group R, n=25), which received remifentanil at 2.0 μg/kg during anesthesia induction followed by continuous infusion of remifentanil at 0.30 μg·kg -1·min -1 for anesthesia maintenance during surgery; a nalbuphine+remifentanil group (group NR, n=23), which was administered with 0.1 mg/kg nalbuphine 15 min before anesthesia induction, then received 2.0 μg/kg remifentanil during anesthesia induction, before continuous infusion of remifentanil at 0.30 μg·kg -1·min -1 for anesthesia maintenance during surgery; and a nalbuphine+parecoxib+remifentanil group (group NPR, n=25), which received 0.05 mg/kg nalbuphine and 40 mg parecoxib 15 min before anesthesia induction, then received 2.0 μg/kg remifentanil during anesthesia induction, before continuous infusion of remifentanil at 0.30 μg·kg -1·min -1 for anesthesia maintenance during surgery. All patients received patient-controlled analgesia pump for postoperative analgesia. The Numerical Rating Scale (NRS) scores at postoperative 1, 3, 6, 12, 24, and 48 h, the consumption of sufentanil at postoperative 3, 6, 12, 24, and 48 h, and the incidence of major adverse reactions such as shivering, nausea and vomiting, drowsiness and dizziness, and skin itching after surgery were recorded. The mechanical pain threshold of the inner forearm and incision side was tested using an electronic Von Frey stimulator before surgery and 24 h after surgery. Results:Compared with groups S, NR, and NPR, group R showed increases in NRS scores at postoperative 1, 3, 6, 12, and 24 h ( P<0.05), increases in the cumulative consumption of sufentanil at postoperative 3, 6, 12, 24, and 48 h ( P<0.05), and decreases in mechanical pain threshold at the incision site and inner forearm at postoperative 24 h ( P<0.05). The mechanical pain threshold of group NR was lower than that of group NPR ( P<0.05). There was no statistical difference in the incidence of shivering, nausea and vomiting, drowsiness and dizziness, and skin itching among the four groups ( P>0.05). Conclusions:The combined use of nalbuphine and parecoxib can effectively prevent RIH after surgery.

Early monitoring and warning arrangements are effective ways to distinguish infectious agents and control the spread of epidemic diseases. Current testing technologies, which cannot achieve rapid detection in the field, have a risk of slowing down the response time to the disease. In addition, there is still no epidemic surveillance system, implementing prevention and control measures is slow and inefficient. Motivated by these clinical needs, a sample-to-answer genetic diagnosis platform based on light-controlled capillary modified with a photocleavable linker is first developed, which could perform nucleic acid separation and release by light irradiation in less than 30 seconds. Then, on site polymerase chain reaction was performed in a handheld closed-loop convective system. Test reports are available within 20 min. Because this method is portable, rapid, and easy to operate, it has great potential for point-of-care testing. Additionally, through multiple device networking, a real-time artificial intelligence monitoring system for pathogens was developed on a cloud server. Through data reception, analysis, and visualization, the system can send early warning signals for disease control and prevention. Thus, anti-epidemic measures can be implemented effectively, and deploying and running this system can improve the capabilities for the prevention and control of infectious diseases.

Spinal cord injury (SCI), following explosive oxidative stress, causes an abrupt and irreversible pathological deterioration of the central nervous system. Thus, preventing secondary injuries caused by reactive oxygen species (ROS), as well as monitoring and assessing the recovery from SCI are critical for the emergency treatment of SCI. Herein, an emergency treatment strategy is developed for SCI based on the selenium (Se) matrix antioxidant system to effectively inhibit oxidative stress-induced damage and simultaneously real-time evaluate the severity of SCI using a reversible dual-photoacoustic signal (680 and 750 nm). Within the emergency treatment and photoacoustic severity assessment (ETPSA) strategy, the designed Se loaded boron dipyrromethene dye with a double hydroxyl group (Se@BDP-DOH) is simultaneously used as a sensitive reporter group and an excellent antioxidant for effectively eliminating explosive oxidative stress. Se@BDP-DOH is found to promote the recovery of both spinal cord tissue and locomotor function in mice with SCI. Furthermore, ETPSA strategy synergistically enhanced ROS consumption via the caveolin 1 (Cav 1)-related pathways, as confirmed upon treatment with Cav 1 siRNA. Therefore, the ETPSA strategy is a potential tool for improving emergency treatment and photoacoustic assessment of SCI.

We developed a rapid point-of-care (POC) testing device for detecting pathogens. Through multi-device networking and the assistance of artificial intelligence technology, an early monitoring and warning system was developed to prevent and control the spread of epidemic diseases.

目的 探索围术期昼夜节律类型改变与剖宫产后急性疼痛及相关因素的关系.方法 利用2020年11月至2021年9月期间在广东医科大学顺德妇女儿童医院行剖宫产手术的148例患者作双向性队列研究.以分娩前及分娩3 d后清晨型和夜晚型问卷自评表(MEQ?SA)的结果分组,两次结果类别不同的归为暴露组,相同的为对照组.结果 暴露组21例,对照组127例,对照组体质量、BMI较高;在经产妇亚组中,暴露组的体质量、BMI及术后1 d疼痛NRS评分显著高于对照组(P<0.05),在初产妇亚组中,暴露组术后当晚医源性睡眠中断次数显著高于对照组(P<0.05);围术期相关因素logistic回归分析发现:体质量越低(OR=0.93,95％CI:0.89～0.97,P<0.001)、睡眠中断次数越多(OR=1.89,95％CI:1.09～3.27,P=0.024)、术后1 d疼痛NRS评分越高(OR=2.25,95％CI:1.10～4.61,P=0.026),昼夜节律改变的风险越高;术前节律为中间型的患者,昼夜节律改变的风险更低(OR=0.12,95％CI:0.02～0.58,P=0.009).结论 围术期昼夜节律改变与术后急性疼痛、体质量、睡眠中断及术前昼夜节律有关,且在不同产妇之间存在明显异质性.

BACKGROUND:Neurotoxicity induced by local anesthetics (LAs) is potentially life threatening, especially for patients with underlying diseases like diabetes. The anesthetic bupivacaine (Bup) has been reported to induce neurotoxicity mediated by reactive oxygen species (ROS), which is aggravated by hyperglycemia. Krüppel-like factor 9 (KLF9), an axon growth-suppressing transcription factor, plays a key role in neuronal maturation and promotes oxidative stress. This study was designed to investigate whether and how KLF9 regulates ROS levels related to LA neurotoxicity under hyperglycemic conditions.METHODS:Klf9/GFP ShRNA (LV Sh-Klf9) was used to achieve stable Klf9 knockdown in the SH-SY5Y cell line. KLF9-deficient and normal cells were cultured under normal or high-glucose (HG) culture conditions and then exposed to Bup. Cell viability, intracellular and mitochondrial ROS, and mitochondrial membrane potential (ΔΨm) were detected to examine the role of KLF9. Thereafter, KLF9-deficient and normal cells were pretreated with small-interfering RNA targeting peroxiredoxin 6 (siRNA-Prdx6) to determine if PRDX6 was the target protein in HG-aggravated Bup neurotoxicity.RESULTS:The mRNA and protein levels of KLF9 were increased after Bup and hyperglycemia treatment. In addition, cell survival and mitochondrial function were significantly improved, and ROS production was decreased after Sh-Klf9 treatment compared with Sh-Ctrl. Furthermore, the expression of PRDX6 was suppressed by Bup in hyperglycemic cultures and was upregulated in the Sh-Klf9 group. Moreover, the protection provided by KLF9 deficiency for cell survival, the increase in ROS production in cells and mitochondria, and the disruption of mitochondrial function were abolished by Prdx6 knockdown.CONCLUSIONS:The results of this study demonstrated that hyperglycemia aggravated Bup neurotoxicity by upregulating KLF9 expression, which repressed the antioxidant PRDX6 and led to mitochondrial dysfunction, ROS burst, and cell death. Understanding this mechanism may, thus, offer valuable insights for the prevention and treatment of neurotoxicity induced by LAs, especially in diabetic patients.

The effects of general anesthetics on the developing brain have aroused much attention in recent years. Sevoflurane, a commonly used inhalation anesthetic especially in pediatric anesthesia, can induce developmental neurotoxicity. In this study, the differentially expressed mRNAs in the hippocampus of newborn rats exposed to 3% sevoflurane for 6 h were detected by RNA-Sequencing. Those data indicated that the mRNA of Klotho was increased after exposure to sevoflurane. Moreover, the protein expression of Klotho was assayed by Western Blot. Besides over-expression and under-expression of Klotho protein, we also detected changes of cell proliferation, ROS, JC-1, and Bcl-2/Bax ratio in PC12 cells exposed to sevoflurane. After exposure to 3% sevoflurane, the expression of Klotho protein increased in the hippocampus of neonatal rats. In PC12 cells, exposure to sevoflurane could increase cellular ROS level, reduce mitochondrial membrane potential and Bcl-2/Bax ratio. While overexpression of Klotho alleviated the above changes, knockdown of Klotho aggravated the injury of sevoflurane. Klotho protein could reduce oxidative stress and mitochondrial injury induced by sevoflurane in the neuron.

Background: Bupivacaine (BP) is commonly used as a local anaesthetic(LA) in the clinic, but it can also cause neurotoxicity, especially in patients with diabetes. Previous studies have found that high-glucose environments can aggravate BP-induced DNA damage in nerve cells. Ku70 is subunit of the DNA damage repair enzyme DNA-PK. This study was designed to determine whether high-glucose conditions enhance BP neurotoxicity and DNA damage by inhibiting Ku70 expression. Methods: We examined the effect of BP on apoptosis and DNA damage in murine dorsal root ganglion (DRG) neurons under hyperglycaemic conditions. Untreated DRG cells and DRG cells pretreated with NU7441, a DNA-PK inhibitor, were cultured for 3 days under normal culture conditions or with 50 mM glucose, and the cells were then treated with BP for 3 h. DNA damage was investigated via comet assays, the ratio of early to late apoptotic cells was assessed by Annexin V-FITC/PI staining, and cell viability was measured by CCK-8 assays. The protein expression levels of DNA-PK, Ku70, Bax, Bcl-2 and gamma H2ax were measured by immunofluorescence or Western blotting. Results: Compared to its effect under normal culture conditions, BP treatment led to decreased cell viability and increased DNA damage in DRG cells grown under high-glucose conditions. The rate of DRG cell apoptosis and the expression of gamma H2ax, the ratio of Bax to Bcl-2 also increased under the high-glucose conditions. Furthermore, Ku70 expression was inhibited. The DNA-PK inhibitor, NU7441, could significantly inhibit DNA-PK and Ku70 expression, simultaneously further aggravating BP-induced apoptosis and DNA damage under high-glucose conditions. Conclusion: These data indicate that hyperglycaemia may enhance BP-induced neurotoxicity and DNA damage by inhibiting the DNA repair protein Ku70.