Objective To analyze the expression of monocyte surface antigen-presenting factors CD86+and HLA-DR in the subacute phase of burn injury,and the molecular mechanism of monocytes contributing to persistent inflammation.Methods The mice were divided into the sham group and the burn group,and a mouse model of 30％body surface burn was estab-lished.Spleens were collected from mice on the 8th day after burn injury,and monocytes were isolated for transcriptomic analy-sis.A mouse model of Notch1 lentiviral transfection was constructed,and models of sham burn+blank control(sham-NC),burn+blank control(burn-NC),sham burn+Notch1 shRNA(sham-sh),and burn+Notch1 shRNA(burn-sh)were estab-lished.The qRT-PCR and Western blot were used to detect the expressions of monocyte surface antigens CD86+and HLA-DR.Immunofluorescence was performed to analyze the expression of CD86+and HLA-DR in splenic monocytes.ELISA was used to analyze serum levels of IL-10 and CRP.Results On the 8th day after burn injury,compared with the sham burn group,the expressions of monocyte surface antigens CD86+and HLA-DR were decreased,while serum levels of IL-10 and CRP were increased in the burn group.Contents of IL-10 and CRP showed significant negative correlations with CD86+and HLA-DR,re-spectively.Transcriptomic analysis revealed 258 significantly upregulated genes and 360 significantly downregulated genes in splenic monocytes from the burn group.The differentially expressed genes primarily enriched in the Notch signaling path-way.Western blot results showed a significant upregulation of Notch1 expression.After lentiviral inhibition of Notch1 signaling invivo,compared with the burn-NC group,expressions of CD86+and HLA-DR on monocyte surfaces were increased,and ser-um levels of IL-10 and CRP were decreased in the burn-sh group.Conclusion The functional inhibition of splenic monocytes is mediated by Notch1 signaling pathway in the subacute phase of burn injury.Inhibition of Notch1 signaling in vivo improves the antigen-presenting capacity of monocytes after burn injury and inhibits the secretion of inflammatory factors.

Objective To analyze the expression of monocyte surface antigen-presenting factors CD86+and HLA-DR in the subacute phase of burn injury,and the molecular mechanism of monocytes contributing to persistent inflammation.Methods The mice were divided into the sham group and the burn group,and a mouse model of 30％body surface burn was estab-lished.Spleens were collected from mice on the 8th day after burn injury,and monocytes were isolated for transcriptomic analy-sis.A mouse model of Notch1 lentiviral transfection was constructed,and models of sham burn+blank control(sham-NC),burn+blank control(burn-NC),sham burn+Notch1 shRNA(sham-sh),and burn+Notch1 shRNA(burn-sh)were estab-lished.The qRT-PCR and Western blot were used to detect the expressions of monocyte surface antigens CD86+and HLA-DR.Immunofluorescence was performed to analyze the expression of CD86+and HLA-DR in splenic monocytes.ELISA was used to analyze serum levels of IL-10 and CRP.Results On the 8th day after burn injury,compared with the sham burn group,the expressions of monocyte surface antigens CD86+and HLA-DR were decreased,while serum levels of IL-10 and CRP were increased in the burn group.Contents of IL-10 and CRP showed significant negative correlations with CD86+and HLA-DR,re-spectively.Transcriptomic analysis revealed 258 significantly upregulated genes and 360 significantly downregulated genes in splenic monocytes from the burn group.The differentially expressed genes primarily enriched in the Notch signaling path-way.Western blot results showed a significant upregulation of Notch1 expression.After lentiviral inhibition of Notch1 signaling invivo,compared with the burn-NC group,expressions of CD86+and HLA-DR on monocyte surfaces were increased,and ser-um levels of IL-10 and CRP were decreased in the burn-sh group.Conclusion The functional inhibition of splenic monocytes is mediated by Notch1 signaling pathway in the subacute phase of burn injury.Inhibition of Notch1 signaling in vivo improves the antigen-presenting capacity of monocytes after burn injury and inhibits the secretion of inflammatory factors.

Existing traditional Chinese medicine (TCM)-related databases are still insufficient in data standardization, integrity and precision, and need to be updated urgently. Herein, an Encyclopedia of Traditional Chinese Medicine version 2.0 (ETCM v2.0, http://www.tcmip.cn/ETCM2/front/#/) was constructed as the latest curated database hosting 48,442 TCM formulas recorded by ancient Chinese medical books, 9872 Chinese patent drugs, 2079 Chinese medicinal materials and 38,298 ingredients. To facilitate the mechanistic research and new drug discovery, we improved the target identification method based on a two-dimensional ligand similarity search module, which provides the confirmed and/or potential targets of each ingredient, as well as their binding activities. Importantly, five TCM formulas/Chinese patent drugs/herbs/ingredients with the highest Jaccard similarity scores to the submitted drugs are offered in ETCM v2.0, which may be of significance to identify prescriptions/herbs/ingredients with similar clinical efficacy, to summarize the rules of prescription use, and to find alternative drugs for endangered Chinese medicinal materials. Moreover, ETCM v2.0 provides an enhanced JavaScript-based network visualization tool for creating, modifying and exploring multi-scale biological networks. ETCM v2.0 may be a major data warehouse for the quality marker identification of TCMs, the TCM-derived drug discovery and repurposing, and the pharmacological mechanism investigation of TCMs against various human diseases.

ObjectiveTo elucidate the mechanism of Osteoking against fracture， femoral head necrosis， osteoarthritis， and lumbar disc herniation by integrating heterogeneous information network mining and experimental validation. MethodOn the basis of the disease-related database and transcriptome expression profiling dataset， as well as the ETCM database， the gene sets related to four target diseases and the candidate target spectrum of Osteoking were obtained through the integration and analysis of bioinformatics data， and a "disease-syndrome-formula-target-pathway-effect" heterogeneous information network was constructed. In addition， by functional enrichment analysis， the core targets of Osteoking in interfering with the imbalance network of four kinds of bone injury diseases， the biological pathways involved， and the corresponding clinical symptoms were screened， and they were verified in animal experiments. ResultHeterogeneous information network mining indicates that Osteoking may commonly reverse the imbalance networks of fracture， femoral head necrosis， osteoarthritis， and lumbar disc herniation via regulating cell function and activity， inhibiting inflammatory response， reducing bone destruction， and improving the immune function of the body by modulating relevant core candidate targets such as RAC-alpha serine/threonine-protein kinase （Akt1）， catenin beta-1 （CTNNB1）， epidermal growth factor receptor （EGFR）， heat shock protein 90-alpha （HSP90AA1）， and phosphatidylinositol 3-kinase catalytic subunit alpha isoform （PI3KCA）， as well as related biological pathways such as phosphatidylinositide 3-kinases/protein kinase B （PI3K/Akt）， janus kinase/signal transducer and activator of transcription （JAK/STAT）， tumor necrosis factor （TNF）， nuclear factor kappa-B （NF-κB）， and Toll-like receptors. In particular， Osteoking may improve the blood supply of the fracture end by regulating blood circulation at the target site of the disease， and it may maintain the balance of bone metabolism by regulating hormone-related pathways to promote fracture healing. In addition， Osteoking may relieve lipid metabolism disorders by targeting and regulating lipid-related pathways， accelerate bone formation and bone repair， and delay the progression of femoral head necrosis. Osteoking may relieve the symptoms of pain by acting on neurological pathways to reduce local nociceptive stimulation in patients with osteoarthritis and lumbar disc herniation. Further experimental validation demonstrates that the PI3K/Akt signaling pathway is the most significantly enriched pathway for the key network targets of Osteoking for the four diseases. The candidate target of Osteoking may have the strongest association with the network of fracture-related genes. Therefore， this study chooses fracture as the target disease to verify the efficacy of Osteoking. The results show that Osteoking can accelerate bone formation and promote fracture healing by inhibiting the activation of the PI3K/Akt signaling axis. ConclusionThe study shows that the main mechanism of "treating different diseases with an identical treatment" of four bone injury diseases with Osteoking involves cell function regulation and immune inflammation-related signaling pathways. Further experimental validation identifies that the PI3K/Akt signaling axis may be one of the key pathways of Osteoking to promote bone regeneration， bone reconstruction， and bone metabolism homeostasis.

ObjectiveTo investigate the clinical efficacy and mechanisms of Osteoking in the treatment of knee osteoarthritis （KOA） in real-world practice， so as to provide a basis for the rational clinical use of Osteoking. MethodFrom the Osteoking for knee osteoarthritis case registration system， 638 KOA cases treated with Osteoking were selected and analyzed in SPSS 26.0. The clinical data were collected from 20 hospitals in China from May 2020 to December 2021. Descriptive analyses of patient age， gender， body mass index， course of treatment and other parameters were performed. The Mann-Whitney U test was performed to compare the visual analogue scale （VAS） and Western Ontario and McMaster universities arthritis index （WOMAC） scores before and after treatment. The integrative pharmacology-based research platform of traditional Chinese medicine （TCMIP） v2.0 was used for network analysis of the core targets of Osteoking in treating knee osteoarthritis. Furthermore， 20 KOA patients treated with Osteoking in the Third Affiliated Hospital of Beijing University of Chinese Medicine from October to December in 2022 were enrolled in the treatment group， and 20 healthy volunteers in the control group. The enzyme-linked immunosorbent assay was employed to measure the serum levels of related indicators to verify the prediction results. ResultA total of 638 KOA patients were treated with Osteoking， including 429 （67.24%） receiving Osteoking alone and 209 （32.76%） receiving Osteoking combined with other therapies. The female patients （415， 65.05%） were more than the male patients （223， 34.95%）. The patients showed the mean age of （63.48±13.51） years， mean body mass index of （24.09±2.98） kg·m^-2， and mean course of treatment of （15.78±9.66） days. Most of the patients were rated as grades Ⅱ （46.24%） and Ⅲ （34.64%） in Kellgren-Lawrence （K-L） grading and in the relief stage （82.45%） in clinical staging. There was no significant correlation between clinical staging and K-L grading results. The cluster analysis identified three TCM syndromes： Qi stagnation and blood stasis， cold-dampness obstruction， and liver-kidney deficiency. The overall clinical efficacy evaluation showed that VAS score decreased from （6.01±0.85） scores before treatment to （2.54±1.73） scores after treatment （P<0.05）， and the WOMAC score decreased from （93.25±25.91） scores before treatment to （50.73±25.14） scores after treatment （P<0.05）. The network analysis predicted that Osteoking might regulate the transforming growth factor-beta （TGF-β）， tumor necrosis factor-alpha （TNF-α）， and nuclear factor-kappa B （NF-κB） signaling pathways to exert the therapeutic effect. The clinical trial showed elevated TGF-β₁ level （P<0.01） and lowered NF-κB subunit RELA and tumor necrosis factor receptor superfamily， member 1A （TNFRSF1A） levels （P<0.05） after treatment. The synergistic effects of these changes provide a multidimensional and comprehensive therapeutic efficacy for KOA， alleviating the joint pain and limited mobility in patients. ConclusionOsteoking showed significant therapeutic efficacy in treating KOA. Osteoking may act on multiple pathways involved in cartilage metabolism and inflammation. The findings provide experimental evidence and theoretical support for elucidating the multi-target mechanism of Osteoking in treating KOA.

ObjectiveTo investigate the improvement of the efficacy of Osteoking in patients with knee osteoarthritis in the onset and remission stage and to systematically explore its potential intervention mechanism， so as to provide a certain reference for improving the clinical application value of Osteoking and guiding its clinical rational drug use. MethodThrough the real-world study of the treatment of knee osteoarthritis with Osteoking， the data was obtained and entered into the "Osteoking for the treatment of knee osteoarthritis case registration system"， and 105 patients with episodic and remission knee osteoarthritis from the outpatient or inpatient orthopedic department of 20 medical institutions， including the Third Affiliated Hospital of Beijing University of Chinese Medicine， Peking Union Medical College Hospital， Wangjing Hospital of the Chinese Academy of Chinese Medical Sciences and Hunan Aerospace Hospital， from May 1， 2020 to December 31， 2021， were selected in the system. It included 60 patients treated with Osteoking and joint injection， and 45 patients treated with joint injection alone. The WOMAC osteoarthritis index score， visual analogue （VAS） pain score， individual types of pain symptoms （cold pain， hot pain， tingling， dull pain， soreness） and other TCM symptoms were observed and compared between the two groups， and statistically analyzed. In order to further elucidate the potential molecular mechanism of Osteoking combined with joint injection in the treatment of knee osteoarthritis in the treatment of onset and remission， this study used the "Bone Injury Cross Database （http：//bone-xtrans.com/database，BX-Data）" to collect the gene set of knee osteoarthritis disease， the traditional Chinese medicinal materials， chemical composition， material base， candidate target， candidate target， sodium hyaluronate candidate target data for screening， and constructed an interaction network of "disease target". ResultsAmong the 105 patients with knee osteoarthritis enrolled， 15.24% （16/105） were in the episodic period， 84.76% （89/105） were in remission， and there were no convalescent patients. There were 72 cases （68.57%） in women， 33 cases （31.43%） more than men， 60 cases in the observation group and 45 cases in the control group in 105 patients. There were 20 patients with a VAS score of 5 and 19 patients with a score of 6 in the observation group， accounting for 65.00% of the observation group. The comparative results of VAS scores between groups before and after treatment showed that the scores of the two groups were （4.42±1.01） scores， （5.00±1.02） scores.4 weeks after treatment， and （3.12±1.04） scores and （3.56±1.08） scores，8 weeks after treatment， respectively， which were lower than those before treatment （6.23±1.28） scores，（ 6.02±1.22） scores （P<0.05）， and the comparative results of the pain properties of the two groups showed that the improvement rates before and after thermal pain and tingling in the observation group were 3.3%（2/60） and 16.7%（10/60）， respectively. The control group was 2.2% （1/45）and 15.6%（7/45）［（χ²=4.034、13.583，P<0.05）］， respectively， and the improvement rate of cold pain and soreness in the observation group was 5.0%（3/60） and 3.3%（2/60）， which was higher than that of the control group . The results of comparing the WOMAC scores before and after treatment of the two groups showed that the difference between the stiffness score before and after treatment in the observation group was （1.68±1.42） scores， the difference between the score before and after treatment in the control group was （1.20±1.60） scores （P<0.05）， and the pain score before and after treatment was （3.43±2.88） scores， the difference before and after daily activity score was （12.37±10.21） scores， and the total score before and after treatment was （17.48±12.76） scores， which were also higher than those in the control group （2.82±3.29）， （10.80±9.63），（14.82±12.62） scores. The results of comparing the improvement of other symptoms before and after treatment showed that the improvement rate of less sleep and more dreams in the observation group was 28.3%（17/60）， which was significantly higher than that of the control group of 2.2%（1/45）（χ²=5.914，P<0.05）， and the improvement rates of the five symptoms of thirst and drinking， irritability， dry mouth and pharynx， dull complexion and hand， foot and mouth fever in the observation group were 3.3%（2/60）， 10.0%（6/60）， 8.3%（5/60）， 10.0%（6/60） and 5.0%（3/60）， respectively， which were higher than those in the control group -2.2%（1/45）， 2.2%（1/45）， 2.2%（1/45）， 4.5%（2/45）， -6.7%（3/45）. Through network analysis， it was found that the enrichment pathway of Henggu bone wound healing agent mainly acted on the three mechanisms of bone improvement， energy metabolism and anti-inflammatory and analgesic， and the sodium hyaluronate enrichment pathway mainly acted on the anti-inflammatory and analgesic mechanism. ConclusionThe efficacy of Osteoking combined with intra-articular injection of sodium hyaluronate in the treatment of patients with knee osteoarthritis in attack and remission is better than that of sodium hyaluronate alone， especially in anti-inflammatory and analgesic， and the two drugs have synergistic effect. Osteoking may play its role in relieving the symptoms of joint stiffness， tingling， heat pain， and less sleep and more dreams by improving bone quality and regulating the body's energy metabolism pathways， which is worthy of clinical promotion.

ObjectiveTo explore the clinical efficacy of Osteoking combined with non-steroidal anti-inflammatory drugs in the treatment of knee osteoarthritis based on real-world data and provide a basis for clinical medication. MethodFrom May 2020 to December 2021， the data of a total of 1 002 patients with knee osteoarthritis who did not undergo knee joint replacement surgery was collected through the registration method. 952 patients were ultimately included， including 133 cases orally taking Osteoking combined with non-steroidal anti-inflammatory drugs as the observation group and 73 cases orally taking non-steroidal anti-inflammatory drugs alone as the control group. Statistical analysis was conducted on the baseline data， VAS scores， WOMAC scores， and other items. The visit point is the 4^th and 8^th weeks after registration. In order to further elucidate the clinical efficacy of Osteoking combined with non-steroidal anti-inflammatory drugs in the treatment of knee osteoarthritis， the effective components of Osteoking and the relevant gene sets of non-steroidal anti-inflammatory drugs and knee osteoarthritis were obtained through network pharmacology methods and retrieval in bone injury cross database， TCMSP， and other databases. Venn analysis was performed on the relevant gene sets， and a PPI network diagram was constructed. Then key core targets were screened out， and enrichment GO and KEGG enrichment analyses were conducted. ResultThe VAS score of the observation group decreases by an average of （-2.79±1.206） scores in the 4^th week， which is better than the control group ［（-2.73±1.575） scores， P<0.05］. The VAS score of the observation group decreases by an average of （-3.97±1.308） scores in the 8^th week， which is better than the control group ［（-3.89±1.822） scores， P<0.05］. The total WOMAC score of the observation group decreases by an average of （-52.07±21.677） scores points in the 8^th week， which is significantly better than the control group ［（-46.75±25.368） scores， P<0.05］. The observation group has an average decrease of （-10.99±4.229） scores in WOMAC （pain） score in the 8^th week， which is better than the control group ［（-10.03±5.535） scores， P<0.05］. The observation group has an average decrease of （-1.49±2.901） in WOMAC （stiffness） score in the 4^th week， which is better than the control group ［（-0.92±1.998） scores， P<0.05］， and the observation group has an average decrease of （-1.90±3.200） scores in WOMAC （stiffness） score in the 8^th week， which is better than the control group ［（-1.26±2.230） scores， P<0.05］. The observation group shows an average decrease of （-39.17±16.562） scores in WOMAC （joint function） score in the 8^th week， which is significantly better than the control group ［（-35.47±20.098） scores， P<0.05］. According to network pharmacology analysis， the core network target of Osteoking in treating knee osteoarthritis is manifested as regulating signal pathways such as signal transduction transcription activator 3（STAT3）， vascular endothelial growth factor A（VEGFA）， tumor necrosis factor （TNF） to regulate cell signaling， angiogenesis， chondrocyte proliferation and migration， and inflammatory cells， thereby inhibiting inflammatory reactions， reducing damage， and delaying the development of the disease. ConclusionAfter a 4-week and 8-week course of treatment for knee osteoarthritis with Osteoking combined with non-steroidal anti-inflammatory drugs， there is a significant therapeutic effect on relieving pain and joint stiffness and improving joint function. In network pharmacology， Osteoking is involved in regulating inflammatory factors， metabolic response-related biological processes， the proliferation and apoptosis of chondrocytes， etc. in the treatment of knee osteoarthritis， resulting in anti-inflammatory and analgesic effects and improving joint mobility and joint stiffness. Therefore， it is worthy of clinical promotion and application.

Objective To examine role and possible mechanism of enriched environment (EE) on regulating recovery of visual function in adult monocular deprivation amblyopia mice.Methods A total of 72 healthyKunming mice were divided into normal control group,monocular deprivation (MD) group,MD+EE group and M D+ fluoxetine group by random number table.Except for the normal control group,the mice in the other groups were sutured on the right eyelid 21 days after birth to establish MD amblyopia model.the mice were fed in standard environment or EE for 4 weeks according to the group.Visual acuity and flash visual evoked potential (F-VEP) of mice in each group were detected.The distribution of microtubule associated protein 2 (MAP2) in visual cortex of adult amblyopic mice were detected by immunohistochemistry.The expression of MAP2,synaptophysin (SYP) and postsynaptic density protein-95 (PSD-95) protein in visual cortex of adult amblyopic mice were detected by western blot.The experimental protocol was approved by the Animal Care and Use Committee of Hunan Children's Hospital and conformed to the National Institutes of Health Guide for the Care and Use of Laboratory Animals.Results There was a significant difference in the visual acuity of deprived eye among each group (F=114.632,P＜0.001).The visual acuity in MD group is lower than that in normal control group,with a significant difference (t =15.480,P＜0.001).Compared with MD group,visual acuity was restored in MD+ EE group and MD +fluoxetine group,with significant differences (t =15.071,P ＜ 0.001;t =14.841,P ＜ 0.001).There was a significant difference in the P2 latency and amplitude of F-VEP in deprived eye among each group (F=36.510,P=0.000;F=34.140,P=0.000).Compare with normal control group,P2 latency was prolonged and P2 amplitude of F-VEP was decreased in deprived eye in MD group,with significant differences (t =10.220,P =0.000;t =10.09,P =0.000).Western blot assay showed that there was a significant difference in the expression of MAP2 in visual cortex contralateral deprived eye among each group (F=18.142,P=0.000).The expression of MAP2 in MD group was significantly lower than that in normal contral group (t=3.056,P＜0.01);Compared with MD group,MAP2 expression was increased in MD+EE group and MD+fluoxetine group (t =2.541,P =0.031;t =2.157,P =0.017).There were significant differences in the expression of SYP and PSD-95 in visual cortex contralateral to deprived eye among each group (F =12.871,P =0.000;F =25.060,P =0.000).Compared with normal contral group,SYP and PSD-95 expression in visual cortex were down-regulated in MD group,with significant differences (t =6.054,P =0.000;t =8.631,P =0.000).The expression of SYP and PSD-95 protein in MD+EE group and MD+fluoxetine group were significantly higher than those in MD group (all at P＜0.05).Conclusions EE can recover visual function through up-regulating the expression of MAP2,which can modulate the dendritic branch trim and neural plasticity of visual cortex in adult MD mice.

Objective: To investigate the situation of quality control of 3.0T magnetic resonance imaging (MRI) system. Methods: A series of indicators, including signal noise ratio(SNR), image uniformity, resolution of long-scale contrast, resolution of space, linearity and quality control of slice thickness, of 3.0T MRI system were measured by using Magphan SMR170 phantom (made by the phantom laboratory in American) on the Discovery MR 750 w system which made by GE company of American. And a series of formula, including SNR=(Sinside-Soutside)÷SDinside, U∑=(1-Smax-Smin/Smax+Smin ×100%, linearity=LR-LM/LR×100%、thickness=half of height and width ×0.25, were used to calculate SNR, image uniformity, linearity and quality control of slice thickness, and all of these results were used to evaluate the situation of quality control of 3.0T MRI system. Results:The results revealed that SNR of 3.0T MRI was 105, the imaging uniformity achieved to 99.13%, the resolution of long-scale contrast was 5mm/0.5mm, the resolution of space was 6 LP/cm, linearity achieved to 0.89% and the deviation of slice thickness was 0.6mm. All of these indicators has achieved the standards of detection. Conclusion: Through detecting the SNR, imaging uniformity, resolution, linearity and the deviation of slice thickness of 3.0T MRI system, the performance of the MRI can be accurately obtained, and these contribute to ensure the equipment operating in ideal situation.

To observe the effect of high-mobility group box 1 (HMGB1) on autophagy and chemotherapy resistance in human leukemiacell line (K562) cells, and to explore the underlying mechanisms.
 Methods: The K562 cells were cultured in vitro and divided into 6 groups: a chemotherapeutic group, a chemotherapeutic control group, a HMGB1 preconditioning group, a HMGB1 preconditioning control group, a HMGB1 siRNA group and a siRNA control group. The chemotherapeutic group was further divided into a vincristine (VCR) group, an etoposide (VP-16) group, a cytosine arabinoside (Ara-C) group, a adriamycin (ADM) group and a arsenic trioxide (As2O3) group. The cell activity was evaluated by cell counting kit-8. The protein levels of HMGB1, microtubule-associate protein1light chain3 (LC3), AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (m-TOR) were determined by Western blotting. The level of serum HMGB1 was evaluated by enzyme-linked immunosorbent assay (ELISA). The autophagy was examined by monodansylcadaverine staining and observed under transmission electron microscopy.
 Results: Compared with the control group, the cell activity was significantly decreased and the level of serum HMGB1 was significantly increased in the chemotherapeutic (VCR, VP-16, Ara-C, ADM and As2O3) groups (all P<0.05). Compared with the control group, the cell activity and the level of serum HMGB1 were significantly increased in the HMGB1 preconditioning group (both P<0.05). Compared with the siRNA control group, the cell activity and the level of serum HMGB1 were significantly decreased in the HMGB1 siRNA group (both P<0.05). Compared with the control group, the expression of LC3-II and the formation of autophagic bodies were increased in the HMGB1 preconditioning group (both P<0.05), the p-AMPK expression was increased and p-mTOR expression was decreased (both P<0.05).
 Conclusion: HMGB1 can increase the autophagy and promote chemotherapy resistance through the pathway of AMPK/m-TOR in K562 cells.
AMP-Activated Protein Kinases ; genetics ; physiology ; Arsenic Trioxide ; Arsenicals ; Autophagy ; genetics ; Cytarabine ; Doxorubicin ; Drug Resistance, Neoplasm ; genetics ; physiology ; Etoposide ; HMGB1 Protein ; genetics ; physiology ; Humans ; K562 Cells ; physiology ; Microtubule-Associated Proteins ; Oxides ; RNA, Small Interfering ; Signal Transduction ; TOR Serine-Threonine Kinases ; genetics ; physiology ; Vincristine