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 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.

Objective:To observe the effects of moxibustion on the levels of glucose-6-phosphate dehydrogenase(G6PD)and reduced nicotinamide adenine dinucleotide phosphate(NADPH)in the plasma and spleen and the CD4+T-cell number in the spleen of rats with adjuvant arthritis,thus to explore the mechanism in rheumatoid arthritis(RA)treatment with moxibustion by regulating the CD4+T-cell proliferation through G6PD-mediated pentose phosphate pathway. Methods:Twenty-seven male Sprague-Dawley rats were randomly divided into a blank group,a model group,and a moxibustion group,with 9 rats in each group.Incomplete Freund's adjuvant was used to induce inflammation in the model group and the moxibustion group.The blank group and the model group were not intervened.In the moxibustion group,suspended moxibustion was performed at bilateral Zusanli(ST36),Guanyuan(CV4),and Ashi points for 30 min,once a day for 24 times in total.Hematoxylin-eosin staining was used to evaluate the histopathological changes of rat synovial tissue;the swelling degree of the rat toes was observed by measuring the toe volume;G6PD and NADPH in the spleen and plasma were detected by Western blotting and enzyme-linked immunosorbent assay.Flow cytometry was used to detect the CD4+T-cell number in the spleen. Results:Compared with the blank group,the levels of G6PD and NADPH in the plasma and spleen and the CD4+T-cell number in the spleen were significantly increased in the model group(P<0.01 or P<0.05).Compared with the model group,the NADPH level in the spleen and plasma and the CD4+T-cell number in the spleen in the moxibustion group decreased significantly(P<0.05 or P<0.01),and the G6PD level in the plasma decreased significantly(P<0.05),but there was no significant difference in the G6PD level in the spleen(P>0.05). Conclusion:Moxibustion can regulate immunity and improve joint synovial inflammation in RA.The mechanism may be that the G6PD-mediated pentose phosphate pathway reduces the production of metabolite NAPDH in CD4+T cells,thereby inhibiting the proliferation of naive CD4+T cells.

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.

AIM: To investigate the differences in varying stages of non-proliferative diabetic retinopathy(NPDR)using optical coherence tomography angiography(OCTA).METHODS: Cross-sectional study. A total of 77 cases(77 eyes)of diabetic patients were included, and they were divided into non-diabetic retinopathy(NDR; 23 eyes)and non-proliferative diabetic retinopathy(NPDR; 54 eyes)groups, further subdivided into mild NPDR(20 eyes), moderate NPDR(20 eyes), and severe NPDR(14 eyes). Foveal avascular zone(FAZ)area, superficial and deep capillary plexus densities(SSP and DSP), and visual acuity(LogMAR)were compared between NDR and NPDR groups. Furthermore, the visual acuity, FAZ area and levels of SSP and DSP were compared in different degrees of NPDR. Correlation analysis were conducted to elucidate relationships between FAZ area, visual acuity, SSP, DSP, and severity of the disease.RESULTS: Compared with the NDR group, the visual acuity(LogMAR)and macular FAZ area increased, while SSP and DSP were decreased in the NPDR group(P<0.05); there were significant differences in visual acuity, FAZ area and SSP and DSP levels in different degrees of NPDR(P<0.05). Visual acuity(LogMAR)and FAZ area displayed a positive correlation with the severity of disease, while SSP and DSP showed a negative correlation.CONCLUSION: With the progression of NPDR, the visual acuity(LogMAR)and FAZ area increased, and the SSP and DSP decreased.

【Objective】 To investigate the application value of 450 nm blue laser vaporization in the treatment of benign prostatic hyperplasia (BPH) in district hospitals, so as to provide reference for the selection of BPH treatment methods in district-level hospitals. 【Methods】 The clinical data of 39 BPH patients who received surgical treatment in Chang’an Hospital during Jan.and Sep.2023 were retrospectively analyzed.The patients were divided into two groups, including 19 in blue laser group treated with 450 nm blue laser vaporization and 20 in the TURP group treated with transurethral resection of the prostate (TURP).The operation time, hemoglobin decline, postoperative bladder irrigation time, catheter indwelling time and adverse events were compared between the two groups. 【Results】 All operations were successfully completed.In the blue laser group, the operation time [(45.11±22.08) min vs.(81.25±29.37) min], postoperative bladder irrigation time [(34.05±9.41) h vs.(47.60±9.05) h] and the decrease of hemoglobin [(7.79± 5.86) g/L vs.(16.40±10.23) g/L] were significantly lower than those in the TURP group (P<0.05).There was 1 case of urinary retention in the blue laser group, and there was no significant difference in indwelling catheter time between the two groups (P>0.05). 【Conclusion】 The 450 nm blue laser vaporization of prostate has advantages of less blood loss, shorter operation time and shorter postoperative irrigation time.Therefore, it should be considered as a preferable option for BPH in primary hospitals.

Objective:To discuss the effects of Buzhong Yiqi Decoction medicated serum combined with cisplatin on the expression of Nrf2 and its effects of downstream antioxidant proteins in human pulmonary adenocarcinoma A549/DDP cells.Methods:Totally 60 rats were divided into blank group, low-dosage group, medium-dosage group, and high-dosage group using a random number table method, with 15 rats in each group. The low-, medium-, and high-dosage groups were orally administered with 3.29, 6.57, and 13.13 g/kg Buzhong Yiqi Decoction for gavage, once a day, for 7 days. 1 hour after the last administration, blood was collected from the abdominal aorta to prepare the serum containing Buzhong Yiqi Decoction. A549/DDP cells were divided into 5 groups: blank group (rat serum), model group (rat serum+cisplatin), low-dosage group (low-dosage Buzhong Yiqi Decoction medicated serum+cisplatin), medium-dosage group (medium-dosage Buzhong Yiqi Decoction medicated serum +cisplatin), and high-dosage group (high-dosage Buzhong Yiqi Decoction medicated serum+cisplatin). And 24 h after the Buzhong Yiqi Decoction intervention, CCK-8 method was used to detect the IC 50 of cisplatin in each group. The fluorescence expression intensity of p-Nrf2 in A549/DDP cells of each group was determined by confocal fluorescence localization method. The mRNA relative expression of Nrf2 in A549/DDP cells of each group was detected by RT-qPCR. The relative expressions of Nrf2, p-Nrf2, GPX4, PRX1 and SOD in A549/DDP cells of each group were detected by Western blot. Results:Compared with the model group, the IC 50 of A549/DDP cells to cisplatin decreased in the low-, medium-, and high-dosage groups ( P<0.01); the fluorescence intensity of p-Nrf2 decreased ( P<0.01); the level of Nrf2 mRNA decreased ( P<0.01); the protein expressions of Nrf2, p-Nrf2, SOD, PRX1, and GPX4 were down-regulated ( P<0.01), with the effect being more significant in the medium- and high-dosage groups ( P<0.05). Conclusion:Buzhong Yiqi Decoction medicated serum can improve cisplatin resistance in human pulmonary adenocarcinoma cancer by inhibiting the active expression of Nrf2 in A549/DDP cells and down-regulating the target genes of SOD, PRX1 and GPX4 in vivo.