Objective: To explore the learning curve of transurethral 450 nm blue light vaporization of the prostate (TUBVP) in a district hospital，in order to provide reference for clinicians who plan to perform TUBVP. Methods: The clinical data of 56 patients with benign prostatic hyperplasia (BPH) who received TUBVP performed by the same group of surgeons in Chang'an District Hospital during Jun. and Dec. 2023 were retrospectively analyzed. Cumulative sum (CUSUM) was used to fit the learning curve of ratio of volume to operating time (RVOT) of prostate volume /450 nm blue light. The learning curve was divided into different stages according to the inflection points，and the clinical data of patients operated at different stages were analyzed and compared. Results: The learning curve of TUBVP was 21 cases，including 1-21 cases in the learning stage，22-38 cases in the improvement stage and 39-56 cases in the maturity stage. With the increase of cases，the postoperative bladder irrigation time reduced \[40.00 (26.00，44.50) h vs. 23.00(20.50，34.00) h vs. 23.50(14.75，40.75) h\]，with statistical difference (P<0.05). The surgical efficiency increased \[(0.51±0.14) vs. (0.55±0.17) vs. (0.63±0.23)\]，while the reduction of hemoglobin \[(6.43±7.35) g/L vs. (5.65±10.91) g/L vs. (2.61±7.36) g/L\]，catheter indwelling time \[70.0 (66.0，106.0) h vs. 71.0 (66.0，89.0) h vs. 66.0 (58.5，78.5) h\]，and incidence of complications (9.5% vs. 5.9% vs. 0) in the three stages showed a gradually decreasing trend，but with no statistical significance (P>0.05). Conclusion: The learning curve of TUBVP is 21 cases. For clinicians in district hospitals，TUBVP is a worthy choice.

ObjectiveTo explore the molecular mechanism of Buzhong Yiqitang in attenuating cisplatin resistance of non-small cell lung cancer （NSCLC） cells （A549/DDP） by regulating endoplasmic reticulum stress （ERS） via the nuclear factor E₂-related factor 2 （Nrf2）/reactive oxygen species （ROS）/double-stranded RNA-activated protein kinase R （PKR）-like endoplasmic reticulum kinase （PERK）/CCAAT enhancer-binding protein homologous protein （CHOP） signaling pathway. MethodsSprague Dawley （SD） rats were used to prepare blank serum and Buzhong Yiqitang-containing serum samples， and A549/DDP cells were sub-cultured and randomly allocated into 9 groups： Blank （10% blank rat serum medium）， model （10% blank rat serum medium+20 mg·L^-1 cisplatin）， traditional Chinese medicine（TCM） （10% Buzhong Yiqitang-containing rat serum medium+20 mg·L^-1 cisplatin）， TBHQ （10% blank rat serum medium+5 μmol·L^-1 TBHQ+20 mg·L^-1 cisplatin）， TBHQ+TCM （10% Buzhong Yiqitang-containing rat serum medium+5 μmol·L^-1 TBHQ+20 mg·L^-1 cisplatin）， NAC （10% blank rat serum medium+600 μmol·L^-1 NAC+20 mg·L^-1 cisplatin）， NAC+TCM （10% Buzhong Yiqitang-containing rat serum medium+600 μmol·L^-1 NAC+20 mg·L^-1 cisplatin）， Salubrinal （10% blank rat serum medium+20 μmol·L^-1 Salubrinal+20 mg·L^-1 cisplatin）， and Salubrinal+TCM （10% Buzhong Yiqitang-containing rat serum medium+20 μmol·L^-1 Salubrinal+20 mg·L^-1 cisplatin）. The median inhibitory concentration （IC₅₀） of cisplatin in each group was determined by the cell counting kit-8 （CCK-8） method. The ROS level was detected by flow cytometry. The ultrastructure of endoplasmic reticulum （ER） was observed by transmission electron microscopy. Western blot was employed to determine the protein levels of Nrf2， phosphorylated （p）-Nrf2， CHOP， PERK， p-PERK， eukaryotic translation initiation factor 2α （eIF2α）， p-eIF2α， and activated transcription factor 4 （ATF4）. The fluorescence intensity of CHOP and p-PERK was detected by confocal fluorescence localization. ResultsCompared with the model group， the TCM group showed a decrease in IC₅₀ of cisplatin in A549/DDP cells （P<0.01）. TBHQ， NAC， and Salubrinal groups showed increases in IC₅₀ of cisplatin in A549/DDP cells （P<0.01）. TCM combined with TBHQ， NAC， and Salubrinal reduced the IC₅₀ （P<0.01）. Compared with that in the blank group， the ROS level in the model group elevated （P<0.01）. Compared with that in the model group， the ROS level in the TCM group elevated （P<0.01）. The ROS levels in the TBHQ， NAC， and Salubrinal groups were lower than that in the model group （P<0.01）. The combinations of TBHQ， NAC， and Salubrinal with TCM raised the ROS levels of A549/DDP cells （P<0.01）. A flat saclike and neatly arranged ER structure was observed in the blank group， and slight expansion of ER was observed in the model group. Significant expansion of ER was observed in the TCM group. The expansion of ER was not obvious in the TBHQ， NAC， and Salubrinal groups but significant after TBHQ， NAC， and Salubrinal were combined with TCM. CHOP and p-PERK showed higher fluorescence intensity in the model group than in the blank group （P<0.01）， and the fluorescence signal intensity in the TCM group was higher than that in the model group （P<0.01）. The fluorescence intensity in the TBHQ， NAC， and Salubrinal groups was lower than that in the model group （P<0.01）. The fluorescence intensity in the groups of TBHQ， NAC， and Salubrinal combined with TCM was higher than that in corresponding groups without TCM （P<0.01）. Compared with those in the blank group， the expression levels of Nrf2 and p-Nrf2 were up-regulated in the model group （P<0.05）. Compared with the model group， the TCM group showed down-regulated expression levels of Nrf2 and p-Nrf2 （P<0.05）. TBHQ， NAC， and Salubrinal increased the expression levels of Nrf2 and p-Nrf2 （P<0.05）， while their combinations with TCM decreased the expression levels of Nrf2 and p-Nrf2 compared with the corresponding groups without TCM （P<0.01）. There were no significant differences in the expression levels of PERK and eIF2α between groups. The expression levels of CHOP， p-PERK/PERK， p-eIF2α/eIF2α， and ATF4 were up-regulated in the model group compared with those in the blank group （P<0.05）. Compared with the model group， the TCM group showed up-regulated expression levels of CHOP， p-PERK/PERK， p-eIF2α/eIF2α， and ATF4 （P<0.05）， while the TBHQ， NAC， and Salubrinal groups showed down-regulated expression levels （P<0.05）. The groups of TBHQ， NAC， and Salubrinal combined with TCM had higher expression levels than the groups without TCM （P<0.01）. ConclusionBuzhong Yiqitang regulates ERS via the Nrf2/ROS/PERK/CHOP signaling pathway to attenuate cisplatin resistance in NSCLC.

ObjectiveTo explore the molecular mechanism of Buzhong Yiqitang in attenuating cisplatin resistance in non-small cell lung cancer （NSCLC） by inducing ferroptosis via poly（rC）-binding protein 1 （PCBP1）. MethodsThe serum containing Buzhong Yiqitang was prepared and cisplatin-resistant human non-small cell lung cancer （NSCLC） cells （A549/DDP） were cultured and randomly grouped as follows： Blank （10% blank serum）， model （10% blank serum+20 mg·L^-1 cisplatin）， Buzhong Yiqitang （10% serum containing Buzhong Yiqitang+20 mg·L^-1 cisplatin）， Fe-1 （10% blank serum+20 mg·L^-1 cisplatin+5 μmol·L^-1 Fe-1）， and Buzhong Yiqitang+Fe-1 （10% serum containing Buzhong Yiqitang+20 mg·L^-1 cisplatin+5 μmol·L^-1 Fe-1）. Firstly， PCR Array was used to screen ferroptosis-related genes regulated by Buzhong Yiqitang， and PCBP1 was identified as the target for studying the attenuation of cisplatin resistance by Buzhong Yiqitang. Subsequently， the median inhibitory concentration （IC₅₀） of cisplatin in each group was determined by the cell counting kit-8 （CCK-8） method and the resistance index （RI） was calculated. The ultrastructure of A549/DDP cells in each group was observed by transmission electron microscopy. The protein levels of PCBP1 and glutathione peroxidase 4 （GPX4） were determined by Western blot. The lipid reactive oxygen species （ROS） content in each group was determined by the C11-BODIRY 581/591 fluorescence probe. The ferrous ion assay kit was used to measure the ferrous ion content in each group. The malondialdehyde （MDA） assay kit was used to determine the MDA content in each group. ResultsCompared with model group， the IC₅₀ of cisplatin and the RI of A549/DDP cells decreased in the Buzhong Yiqitang group （P<0.05） but increased in the Fe-1 group （P<0.05）. The IC₅₀ of cisplatin and the RI of A549/DDP cells in the Buzhong Yiqitang+Fe-1 group were lower than those in the Fe-1 group （P<0.05）. Compared with the model group， the Buzhong Yiqitang group showed obvious mitochondrial ferroptosis， while the mitochondrial damage became less obvious after Fe-1 treatment. Compared with that in the Fe-1 group， the mitochondrial ferroptosis was aggravated after the intervention with Buzhong Yiqitang. Compared with blank group， the model group showed down-regulated expression levels of PCBP1 and GPX4 （P<0.05） and increased content of lipid ROS， ferrous ions， and MDA （P<0.05） in A549/DDP cells. Compared with model group， the Buzhong Yiqitang group showed down-regulated expression levels of PCBP1 and GPX4 （P<0.05） and increased content of lipid ROS， ferrous ions， and MDA （P<0.05）， while the Fe-1 group showed up-regulated expression levels of PCBP1 and GPX4 （P<0.05） and reduced content of lipid ROS， ferrous ions， and MDA （P<0.05）. Compared with the Fe-1 group， the Buzhong Yiqitang+Fe-1 group showed down-regulated expression levels of PCBP1 and GPX4 and increased content of lipid ROS， ferrous ions， and MDA （P<0.05）. ConclusionBuzhong Yiqitang attenuated cisplatin resistance in NSCLC by regulating PCBP1 to induce ferroptosis.

ObjectiveTo investigate the mechanism of Buzhong Yiqitang in attenuating cisplatin resistance in non-small cell lung cancer by observing the effects of Buzhong Yiqitang on endoplasmic reticulum stress-related molecules in human lung adenocarcinoma cells （A549） and cisplatin-resistant cells in human lung adenocarcinoma cells （A549/DDP） via the nuclear factor E₂-related factor 2（Nrf2）/reactive oxygen species（ROS） pathway. MethodsThe serum containing Buzhong Yiqitang was prepared and A549 cells and A549/DDP cells were cultured. The cells were randomized into groups A （A549 cells+blank serum）， B （A549 cells+20 mg·L^-1 cisplatin+blank serum）， C （A549 cells+20 mg·L^-1 cisplatin+10% Buzhong Yiqitang-containing serum）， D （A549/DDP cells+blank serum）， E （A549/DDP cells+20 mg·L^-1 cisplatin+blank serum）， and F （A549/DDP cells+20 mg·L^-1 cisplatin+10% Buzhong Yiqitang-containing serum）. The cell counting kit-8 （CCK-8） method was used to detect the half maximal inhibitory concentration （IC₅₀） of cisplatin. The protein levels of Nrf2 and p-Nrf2 were determined by Western blotting. The DCFH-DA fluorescent probe was used to measure the content of reactive oxygen species （ROS） in each group. The protein levels of glucose-regulated protein 78 （GRP78）， activated transcription factor 6 （ATF6）， and C/EBP-homologous protein （CHOP） were determined by Western blot. ResultsCompared with group B， group C showed a reduction in IC₅₀ of cisplatin （P<0.05）， which held true in group E compared with group F （P<0.05）. Moreover， the IC₅₀ of cisplatin to A549/DDP cells was higher than that to A549 cells before and after Buzhong Yiqitang intervention （P<0.05）. Compared with group A， group B showed up-regulated protein levels of Nrf2 and p-Nrf2 （P<0.05）. Compared with group B， group C showed down-regulated protein levels of Nrf2 and p-Nrf2 （P<0.05）. Compared with group D， group E showed up-regulated protein levels of Nrf2 and p-Nrf2 （P<0.05）， which， however， were significantly down-regulated in group F （P<0.05）. The ROS content and the protein levels of GRP78， ATF6， and CHOP followed a descending trend of group C > group B > group A in A549 cells and group F > group E > group D in A549/DDP cells （P<0.05）. Moreover， the ROS content and the protein levels of GRP78， ATF6， and CHOP in A549 cells were higher than those in A549/DDP cells before and after Buzhong Yiqitang intervention （P<0.05）. ConclusionBuzhong Yiqitang may regulate endoplasmic reticulum stress via the Nrf2/ROS pathway to attenuate cisplatin resistance in non-small cell lung cancer.

In the process of tumor chemotherapy， the emergence of multi-drug resistance （MDR） has always been a thorny problem， which is a result of the joint action of the host， tumor cells， and the immune microenvironment. Tumor cells can escape the toxicity of chemotherapeutic drugs through multiple pathways， being easy to produce drug resistance. MDR greatly restricts the effect of chemotherapeutic drugs on tumor cells and affects their therapeutic effects. Traditional Chinese medicine （TCM） has the unique advantages of multi-target， multi-pathway and individualized treatment. The TCM treatment of tumors emphasizes regulating Yin and Yang， as well as reinforcing healthy Qi and dispelling pathogen. In recent years， TCM has demonstrated remarkable efficacy in the treatment of tumors and the amelioration of multi-drug resistance. TCM not only can target the phenomenon of MDR but also greatly weakens the side effects of the patients after the chemotherapy， thus improving the survival quality and rate of the patients. Accordingly， many patients adopt TCM as an adjuvant therapy during or after chemotherapy. The binding of TCM to targets can reverse the drug resistance of various tumors， which has become an emerging research highlight. From the regulatory mechanism of TCM on MDR of tumors， this paper introduces the mechanisms by which tumor cells continue to grow， proliferate， and metastasize by adjusting the intracellular drug concentration， altering or utilizing the tumor microenvironment， and affecting the cell death mode to achieve the resistance to chemotherapeutic drugs. In this regard， the active ingredients and compound prescriptions of TCM can increase the sensitivity of chemotherapeutic drugs by down-regulating drug transporters， improving the tumor microenvironment， and modulating the drug resistance pathways associated with apoptosis， autophagy， ferroptosis， or pyroptosis. The aim of this paper is to explore more clinical practical value of TCM in the treatment of tumors and provide exploratory ideas and a theoretical basis for the future research on tumors and MDR.

Objective:To explore the changes of brain excitation/inhibition balance and gray matter volume (GMV) and their correlations with clinical features in benign childhood epilepsy with centrotemporal spikes (BECTS).Methods:A cross-sectional study was performed; 83 BECTS children enrolled from Department of Diagnostic Radiology, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University from January 2015 to January 2024 were selected as BECTS group. During the same period, 101 age- and gender-matched healthy children were recruited as healthy control group through advertisements in local primary schools. Data of conventional MRI and resting-state functional MRI (rs-fMRI) of the two groups were collected. Whole brain GMV was analyzed by voxel-based morphometry (VBM), and Hurst index was calculated based on time series data of blood oxygen level dependent (BOLD) signal of rs-fMRI. Correlations of GMV and Hurst index with disease duration and onset age in children with BECTS were explored by Pearson correlation analysis.Results:Compared with the healthy control group, the BECTS group had significantly increased GMV and decreased Hurst index in the bilateral Rolandic region ( P<0.05). Pearson correlation analysis showed that in the BECTS group, GMV in bilateral Rolandic region was negatively correlated with onset age ( r=-0.267, P=0.015) and positively correlated with disease course ( r=0.267, P=0.015); Hurst index in bilateral Rolandic region was positively correlated with onset age ( r=0.323, P=0.003) and negatively correlated with disease course ( r=-0.240, P=0.029); Hurst index was negatively correlated with GMV in bilateral Rolandic region ( r=-0.328, P=0.003). Conclusion:BECTS children have excitation/inhibition imbalance in epilepsy-related regions and cortical structural delay, and both of them are related to onset age and disease course.

Objective:To observe the effect of moxibustion on angiogenesis-related indicators in knee joint synovial tissue of adjuvant arthritis model rats,and to explore the mechanism of moxibustion in inhibiting vascular endothelial growth factor(VEGF)expression in synovial tissue and further limiting the activation of Rho family proteins Rac1 and Cdc42,thereby inhibiting angiogenesis during rheumatoid arthritis(RA)treatment.Methods:Forty-eight male Sprague-Dawley rats were equally divided into a normal group,a model group,a moxibustion group,and a moxibustion+VEGF agonist group according to the random principle.The complete Freund's adjuvant method was used for modeling.On the 12th day after modeling,the moxibustion group and the moxibustion+VEGF agonist group were subjected to suspended moxibustion at bilateral Zusanli(ST36),Guanyuan(CV4),and Ashi points for 20 min each time,once a day,for a total of 15 times.The moxibustion+VEGF agonist group received VEGF agonist(tirofiban hydrochloride hydrate)injection in the knee joint cavity at the same time.Hematoxylin-eosin staining was used to evaluate the pathological changes of rat synovial tissue in each group.Immunohistochemistry was used to observe the CD31 expression level in rat synovial tissue.Western blotting was used to detect the levels of VEGF,Rac1,and Cdc42 protein in rat synovial tissue,and polymerase chain reaction(PCR)was used to detect the VEGF mRNA expression.Results:Compared to the normal group,the expression levels of CD31 protein and VEGF mRNA and protein in rat synovial tissue in the model group increased significantly(P<0.01),and the expression levels of phospho-Rac1 and phospho-Cdc42 proteins also increased significantly(P<0.01).After moxibustion intervention,the expression levels of CD31 protein and VEGF mRNA and protein in the moxibustion group were significantly lower than those in the model group(P<0.01),while the differences in each indicator between the moxibustion+VEGF agonist group and the model group were not statistically significant(P>0.05).Compared to the moxibustion group,the expression levels of CD31 protein,VEGF mRNA and protein,phospho-Cdc42,and phospho-Rac1 in the moxibustion+VEGF agonist group increased significantly(P<0.01).Conclusion:Moxibustion improved synovial inflammation in RA by inhibiting angiogenesis.The mechanism may be to regulate angiogenesis-related VEGF,restrict the activation of Rac1 and Cdc42,and inhibit pseudopodia formation in vascular endothelial cells,thereby reducing angiogenesis.

Objective:To observe the effect of moxibustion on angiogenesis-related indicators in knee joint synovial tissue of adjuvant arthritis model rats,and to explore the mechanism of moxibustion in inhibiting vascular endothelial growth factor(VEGF)expression in synovial tissue and further limiting the activation of Rho family proteins Rac1 and Cdc42,thereby inhibiting angiogenesis during rheumatoid arthritis(RA)treatment.Methods:Forty-eight male Sprague-Dawley rats were equally divided into a normal group,a model group,a moxibustion group,and a moxibustion+VEGF agonist group according to the random principle.The complete Freund's adjuvant method was used for modeling.On the 12th day after modeling,the moxibustion group and the moxibustion+VEGF agonist group were subjected to suspended moxibustion at bilateral Zusanli(ST36),Guanyuan(CV4),and Ashi points for 20 min each time,once a day,for a total of 15 times.The moxibustion+VEGF agonist group received VEGF agonist(tirofiban hydrochloride hydrate)injection in the knee joint cavity at the same time.Hematoxylin-eosin staining was used to evaluate the pathological changes of rat synovial tissue in each group.Immunohistochemistry was used to observe the CD31 expression level in rat synovial tissue.Western blotting was used to detect the levels of VEGF,Rac1,and Cdc42 protein in rat synovial tissue,and polymerase chain reaction(PCR)was used to detect the VEGF mRNA expression.Results:Compared to the normal group,the expression levels of CD31 protein and VEGF mRNA and protein in rat synovial tissue in the model group increased significantly(P<0.01),and the expression levels of phospho-Rac1 and phospho-Cdc42 proteins also increased significantly(P<0.01).After moxibustion intervention,the expression levels of CD31 protein and VEGF mRNA and protein in the moxibustion group were significantly lower than those in the model group(P<0.01),while the differences in each indicator between the moxibustion+VEGF agonist group and the model group were not statistically significant(P>0.05).Compared to the moxibustion group,the expression levels of CD31 protein,VEGF mRNA and protein,phospho-Cdc42,and phospho-Rac1 in the moxibustion+VEGF agonist group increased significantly(P<0.01).Conclusion:Moxibustion improved synovial inflammation in RA by inhibiting angiogenesis.The mechanism may be to regulate angiogenesis-related VEGF,restrict the activation of Rac1 and Cdc42,and inhibit pseudopodia formation in vascular endothelial cells,thereby reducing angiogenesis.

Objective:To explore the changes of brain excitation/inhibition balance and gray matter volume (GMV) and their correlations with clinical features in benign childhood epilepsy with centrotemporal spikes (BECTS).Methods:A cross-sectional study was performed; 83 BECTS children enrolled from Department of Diagnostic Radiology, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University from January 2015 to January 2024 were selected as BECTS group. During the same period, 101 age- and gender-matched healthy children were recruited as healthy control group through advertisements in local primary schools. Data of conventional MRI and resting-state functional MRI (rs-fMRI) of the two groups were collected. Whole brain GMV was analyzed by voxel-based morphometry (VBM), and Hurst index was calculated based on time series data of blood oxygen level dependent (BOLD) signal of rs-fMRI. Correlations of GMV and Hurst index with disease duration and onset age in children with BECTS were explored by Pearson correlation analysis.Results:Compared with the healthy control group, the BECTS group had significantly increased GMV and decreased Hurst index in the bilateral Rolandic region ( P<0.05). Pearson correlation analysis showed that in the BECTS group, GMV in bilateral Rolandic region was negatively correlated with onset age ( r=-0.267, P=0.015) and positively correlated with disease course ( r=0.267, P=0.015); Hurst index in bilateral Rolandic region was positively correlated with onset age ( r=0.323, P=0.003) and negatively correlated with disease course ( r=-0.240, P=0.029); Hurst index was negatively correlated with GMV in bilateral Rolandic region ( r=-0.328, P=0.003). Conclusion:BECTS children have excitation/inhibition imbalance in epilepsy-related regions and cortical structural delay, and both of them are related to onset age and disease course.

ObjectiveTo explore the mechanism of Buzhong Yiqitang-containing serum in alleviating the cisplatin resistance in human non-small cell lung cancer （A549/DDP） cells via regulating the nuclear factor E₂-related factor 2 （Nrf2）/reactive oxygen species （ROS） signaling pathway. MethodThe serum containing Buzhong Yiqitang was prepared and A549/DDP cells were cultured and randomly grouped： blank （10% blank serum）， cisplatin （10% blank serum+20 mg·L^-1 cisplatin）， Buzhong Yiqitang （10% Buzhong Yiqitang-containing serum+20 mg·L^-1 cisplatin）， ML385 （10% blank serum+5 μmol·L^-1 ML385+20 mg·L^-1 cisplatin）， Buzhong Yiqitang+ML385 （10% Buzhong Yiqitang-containing serum+5 μmol·L^-1 ML385+20 mg·L^-1 cisplatin）， tertiary butylhydroquinone （TBHQ） （10% blank serum+5 μmol·L^-1 TBHQ+20 mg·L^-1 cisplatin）， and Buzhong Yiqitang+TBHQ （10% Buzhong Yiqitang-containing serum+5 μmol·L^-1 TBHQ+20 mg·L^-1 cisplatin）. The median inhibitory concentration （IC₅₀） of cisplatin in each group was determined by the cell counting kit-8 （CCK-8） method and the resistance index （RI） was calculated. The apoptosis rate was detected by flow cytometry. The ROS content of each group was determined with the DCFH-DA fluorescence probe. Western blot was employed to determine the protein levels of Nrf2， cleaved cysteinyl aspartate-specific protease-3 （cleaved Caspase-3）， cytochrome C （Cyt C）， and B-cell lymphoma-2 （Bcl-2）. ResultCompared with those in the cisplatin group， the IC₅₀ and RI of A549/DDP cells to cisplatin in Buzhong Yiqitang， ML385， and Buzhong Yiqitang+ML385 groups decreased （P˂0.05）. Compared with the blank group， the cisplatin， Buzhong Yiqitang， ML385， and Buzhong Yiqitang+ML385 groups showed increased apoptosis rate of A549/DDP cells （P˂0.05）. Compared with the blank group， cisplatin promoted the expression of Nrf2 （P˂0.05）. Compared with the cisplatin group， Buzhong Yiqitang， ML385， and Buzhong Yiqitang+ML385 inhibited the expression of Nrf2 （P<0.05）， elevated the ROS level （P˂0.05）， up-regulated the protein levels of cleaved Caspase-3 and Cyt C， and down-regulated the protein level of Bcl-2 （P<0.05）， which were the most significant in the Buzhong Yiqitang+ML385 group. Compared with the cisplatin group， the TBHQ group showed increased IC₅₀ and RI of cisplatin （P<0.05）， decreased apoptosis rate of A549/DDP cells （P<0.05）， up-regulated protein levels of Nrf2 and Bcl-2 （P<0.05）， lowered level of ROS （P˂0.05）， and down-regulated protein levels of cleaved Caspase-3 and Cyt C （P<0.05）. Compared with the TBHQ group， Buzhong Yiqitang+TBHQ decreased the IC₅₀ and RI of cisplatin in A549/DDP cells （P<0.05）， increased the apoptosis rate （P<0.05）， down-regulated the protein levels of Nrf2 and Bcl-2 （P<0.05）， increased ROS （P˂0.05）， and up-regulated the protein levels of cleaved Caspase-3 and Cyt C （P<0.05）. ConclusionBuzhong Yiqitang induced apoptosis by inhibiting Nrf2/ROS pathway to alleviate cisplatin resistance in A549/DDP cells.