The patient, an 11-year-old girl, was admitted with recurrent fever for 20 days, worsening with abdominal distension for 7 days. Upon admission, she presented with recurrent fever, lymphadenopathy, hepatosplenomegaly, polyserositis, and multiple organ dysfunction. Lymph node pathology and clinical manifestations confirmed the diagnosis of idiopathic multicentric Castleman disease-TAFRO syndrome. Treatment with siltuximab combined with glucocorticoids was initiated, followed by maintenance therapy with tocilizumab. The patient is currently in complete clinical remission. Therefore, once a child is diagnosed with idiopathic multicentric Castleman disease -TAFRO syndrome, early use of siltuximab should be considered for rapid disease control, followed by tocilizumab for maintenance therapy.

Vissers-Bodmer Syndrome (VIBOS) is an autosomal dominant disorder caused by variants in the CNOT1 gene. It is characterized by systemic developmental and language-motor delay, intellectual disabilities, growth and behavioral abnormalities, hypotonia, and distal skeletal defects, such as deformities of the hands and feet. This syndrome becomes evident during infancy and can display a highly variable phenotype. Thirty-nine individuals with heterozygous de novo CNOT1 variants were first reported in 2019. Herein, we report a child with VIBOS who exhibited delayed motor development for over 4 years, along with hypotonia and atypical facial features. Notably, the patient developed short stature as the primary characteristic without any intellectual disability or organic nervous system lesions. Genetic testing revealed a de novo base duplication variant in exon 5 of the CNOT1 gene, NM_016284.5(CNOT1):c.316_317dup(p.Pro107Serfs*10). Importantly, the pathogenicity of this specific variant has not been reported in relevant literature. This study reports a new variant, thereby enriching the variant spectrum of CNOT1 associated with VIBOS, and contributes to the genetic counseling of affected families.

Background Solasonine, as a major biological component of Solanum nigrum L., has demonstrated anticancer effects against several malignancies. However, little is understood regarding its biological target and mechanism in non-small cell lung cancer (NSCLC). Methods We conducted an analysis on transcriptomic data to identify differentially expressed genes (DEGs), and employed an artificial intelligence (AI) strategy to predict the target protein for solasonine. Subsequently, genetic dependency analysis and molecular docking were performed, with Acetylcholinesterase (ACHE) selected as a pivotal marker for solasonine. We then employed a range of bioinformatic approaches to explore the relationship between ACHE and solasonine. Furthermore, we investigated the impact of solasonine on A549 cells, a human lung cancer cell line. Cell inhibition of A549 cells following solasonine treatment was analyzed using the CCK8 assay. Additionally, we assessed the protein expression of ACHE, as well as markers associated with apoptosis and inflammation, using western blotting. To investigate their functions, we employed a plasmid-based ACHE overexpression system. Finally, we performed dynamics simulations to simulate the interaction mode between solasonine and ACHE. Results The results of the genetic dependency analysis revealed that ACHE could be identified as the pivotal target with the highest docking affinity. The cell experiments yielded significant findings, as evidenced by the negative regulatory effect of solasonine treatment on tumor cells, as demonstrated by the CCK8 assay. Western blotting analysis revealed that solasonine treatment resulted in the downregulation of the Bcl-2/Bax ratio and upregulation of cleaved caspase-3 protein expression levels. Moreover, we observed that ACHE overexpression promoted the expression of the Bcl-2/Bax ratio and decreased cleaved caspase-3 expression in the OE-ACHE group. Notably, solasonine treatment rescued the Bcl-2/Bax ratio and cleaved caspase-3 expression in OE-ACHE cells compared to OE-ACHE cells without solasonine treatment, suggesting that solasonine induces apoptosis. Besides, solasonine exhibited its anti-inflammatory effects by inhibiting P38 MAPK. This was supported by the decline in protein levels of IL-1β and TNF-α, as well as the phosphorylated forms of JNK and P38 MAPK. The results from the molecular docking and dynamics simulations further confirmed the potent binding affinity and effective inhibitory action between solasonine and ACHE. Conclusions The findings of the current investigation show that solasonine exerts its pro-apoptosis and anti-inflammatory effects by suppressing the expression of ACHE.

目的:总结儿童类固醇糖尿病(SDM)的临床表现、治疗及预后，为其防治提供依据。方法:对2012年3月至2022年3月就诊于中南大学湘雅二医院儿科的14例SDM患儿的临床资料进行回顾性分析，按原发疾病不同分为肾病组和血液系统疾病组。结果:14例SDM患儿，肾病组10例，血液系统疾病组4例，12例患儿起病年龄10~12岁，6例在起病前有大剂量使用糖皮质激素(GCs)史，5例存在糖尿病家族史；1例出现典型多饮、多尿表现；7例患儿空腹血糖正常，所有患儿均存在餐后高血糖；血液系统疾病组空腹、早餐后2 h、晚餐前、凌晨3点末梢血糖均高于肾病组，差异均具有统计学意义(均 P<0.05)；经随访现仅1例确诊持续性糖尿病。 结论:儿童SDM无明显临床症状，以餐后血糖升高为主，高血糖出现时间规律与程度可能与所使用GCs的类型及给药频次有关；SDM预后较好，极少转为持续性糖尿病。

Objective: Polyethylene glycol recombinant human growth hormone (PEG-rhGH, Jintrolong®) is the first long-acting rhGH preparation that is approved to treat children with growth hormone deficiency (GHD) in China. Clinical experience with dose selections of PEG-rhGH is scarce. The present study compared the efficacy and safety of a lower dose to increase dosing regimens of PEG-rhGH treatment. Methods: A multicenter, randomized, open-label, dose-comparison clinical study was conducted to compare the improvements in the height standard deviation score (Ht SDS), height velocity (HV), insulin-like growth factor-1 (IGF-1) SDS, and safety profiles of children with GHD who are treated with 0.2 mg/kg/week of PEG-rhGH dose or 0.14 mg/kg/week for 26 weeks. Results: Ht SDS, HV, and IGF-1 SDS increased significantly after PEG-rhGH treatment in the two dose groups (p < 0.05). The improvements of Ht SDS, HV, and IGF-1 SDS were more significant in the high-dose group than in the low-dose group (p < 0.05). Ht SDS improvement in low-dose group was not non-inferiority to that in the high-dose group (p = 0.2987). The incidences of adverse events were comparable between the two groups. Conclusion: The improvements of Ht SDS, HV, and IGF-1 SDS were more significant in the high-dose group than in the low-dose group (p < 0.05). PEG-rhGH at the dose of 0.14 mg/kg/week was effective and safe for children with GHD. Clinical Trial Registration: clinicaltrials.gov, identifier NCT02908958.

Objective To investigate the mechanism of the Qibaipingfei Capsule regulating chronic obstructive pulmonary (COPD) related immune cells by analyzing the single-cell transcriptome sequencing (scRNA-seq) data of COPD lung tissue and the pharmacology of Qibaipingfei Capsule. Methods The scRNA-seq data of COPD lung tissue downloaded from the gene expression omnibus (GEO) was used to obtain the COPD related immune cells and the differentially expressed RNA, and the primary active molecular and target genes of Qibaipingfei Capsule were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). The "active molecules-immune cells-target genes" network was constructed by mapping the target genes of Qibaipingfei Capsules to the differentially expressed RNA of COPD related immune cells, and the Gene Ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and the protein-protein interaction (PPI) were administrated to analyze the molecular mechanisms of target genes. Results Twelve active molecules including quercetin, kaempferol, and formononetin of Qibaipingfei Capsule targeted multiple COPD related immune cells like macrophages, alveolar macrophages, and T cells, and genes like PPARG, JUN, HMOX1, and HIF1A which were primarily collected in pathways such as interleukin 17 signaling pathway, nuclear factor-κB (NF-κB) signaling pathway, and mitogen-activated protein kinase (MAPK) signaling pathway. Conclusions The Qibaipingfei Capsule may target multiple immune cells and intervene in inflammation and immune-related pathways to regulate the inflammation and immune response of COPD.

OBJECTIVE:Qiyusanlong (QYSL) formula has been used in the clinic for more than 20 years and has been proved to have pronounced efficacy in the treatment of non-small-cell lung cancer (NSCLC). This work aims to evaluate the molecular mechanism of QYSL formula action on NSCLC, specifically in relation to autophagy induction.METHODS:In vitro, CCK-8 was used to detect the effect of QYSL serum on cell viability in A549 cells. In vivo, A549 cells were implanted subcutaneously in nude mice to establish a xenograft model. TUNEL staining was used to measure cell apoptosis and TEM to observe the autophagy-related morphological changes in vitro and in vivo. Western blotting, RT-qPCR, and immunofluorescence were used to measure autophagy-related proteins. In addition, rapamycin (an inhibitor of mTOR and inducer of autophagy) and MHY1485 (an activator of mTOR and inhibitor of autophagy) were used to determine whether QYSL-induced autophagy was regulated by the mTOR pathway.RESULTS:QYSL serum inhibited the cell viability of A549 cells in a concentration-dependent manner. In vivo, the QYSL formula inhibited xenograft growth. The QYSL formula promoted apoptosis in A549 cells and induced autophagosome formation in vitro and in vivo. In addition, the QYSL formula downregulated the expression of mTOR and p62, while it upregulated the expression of ATG-7 and Beclin-1 and increased the LC3-II/LC3-I ratio. QYSL serum inhibited p-mTOR in a similar manner to rapamycin while reducing the activating effects of MHY1485 on p-mTOR.CONCLUSION:The QYSL formula has anti-lung cancer effects and promotes autophagy through the mTOR signaling pathway.

Abstract Background Leigh syndrome, the most common mitochondrial syndrome in pediatrics, has diverse clinical manifestations and is genetically heterogeneous. Pathogenic mutations in more than 75 genes of two genomes (mitochondrial and nuclear) have been identified. PDHA1 encoding the E1 alpha subunit is an X‐chromosome gene whose mutations cause pyruvate dehydrogenase complex deficiency. Methods Here, we have described a 12‐year‐old boy with lethal neuropathy who almost died of a sudden loss of breathing and successive cardiac arrest. Extracorporeal membrane oxygenation rescued his life. His diagnosis was corrected from Guillain–Barré syndrome to Leigh syndrome 1 month later by clinical exome sequencing. Furthermore, we used software to predict the protein structure caused by frameshift mutations. We treated the boy with vitamin B1, coenzyme Q10, and a ketogenic diet. Results A PDHA1 mutation (NM_000284.4:c.1167_1170del) was identified as the underlying cause. The amino acid mutation was p.Ser390LysfsTer33. Moreover, the protein structure prediction results suggested that the protein structure has changed. The parents of the child were negative, so the mutation was de novo. The comprehensive assessment of the mutation was pathogenic. His condition gradually improved after receiving treatment. Conclusion This case suggests that gene detection should be popularized to improve diagnosis accuracy, especially in developing countries such as China.

Genistein, a naturally occurring phytoestrogen and a member of the large class of compounds known as isoflavones, exerts protective effects in several diseases. Recent studies indicate that genistein plays a critical role in controlling body weight, obesity-associated insulin resistance, and metabolic disorders, but its target organs in reversing obesity and related pathological conditions remain unclear. In this study, we showed that mice supplemented with 0.2% genistein in a high-fat diet for 12 weeks showed enhanced metabolic homeostasis, including reduced obesity, improved glucose uptake and insulin sensitivity, and alleviated hepatic steatosis. We also observed a beiging phenomenon in the white adipose tissue and reversal of brown adipose tissue whitening in these mice. These changes led to enhanced resistance to cold stress. Altogether, our data suggest that the improved metabolic profile in mice treated with genistein is likely a result of enhanced adipose tissue function.

Objective:To investigate the behavioral problems of children with congenital adrenal hyperplasia (CAH), and to explore the influencing factors, thus providing evidence for their prevention and interventions.Methods:A case-control study was carried out.A total of 25 children with CAH who were aged 4-16 and regularly followed up in the Outpatient Department of the Second Xiangya Hospital, Central South University from June 1, 2017 to March 31, 2019 were enrolled in the study group, and 50 age-and gender-matched healthy children in Hunan Province were selected as the healthy control group.The parents of the selected subjects were investigated with the Achenbach Child Behavior Checklist (CBCL) to evaluate children′s behavior problems.SPSS 22.0 software was applied to statistical analysis.Results:(1) The scores of externalizing behaviors, aggressive factors and behavior problems in 4-to 5-year-old male children in the CAH group were significantly higher than those in the healthy control group [(12.440±8.353) scores vs.(5.060±5.230) scores, (9.670±6.481) scores vs.(4.110±4.157) scores, (22.110±13.062) scores vs.(12.890±9.405) scores] ( t=2.829, 2.711, 2.109, respectively, all P<0.05). There was no significant difference in the scores of other behavior problems and influencing factors between the CAH group and the healthy control group (all P>0.05). (2) The influencing factor of behavioral problems was progesterone ( β=0.567). Testoste-rone not only was the influencing factor of externalizing and internalizing behaviors ( β=0.582, 0.497, respectively), but also affected the behavior of physical complaints, violation of discipline and social withdrawal ( β=0.735, 0.531 and 0.492, respectively). The factor influencing the schizoid behavior was the initial treatment age ( β=0.402). Conclusions:Four- to 5-year-old male children with CAH have behavioral problems, among which aggression and externalizing behaviors are more common.The increase of testosterone may cause the problems of internalizing and externalizing behaviors in children with CAH, and has a great impact on physical complaints, social withdrawal, and discipline violation.The increase of progesterone may lead to the behavior problems of the children.The older the initial treatment age, the more serious the schizoid behavior problem may be.

Objective:To investigate the clinical characteristic, gene mutations and genotype-phenotype correlation of 21-hydroxylase deficiency (21-OHD) in Hunan.Methods:A total of 48 patients with 21-OHD who were admitted to the Department of Pediatrics, the Second Xiangya Hospital, Central South University from March 2016 to March 2017 were collected.According to the clinical manifestations and biochemical characteristics of the patients, they were divided into salt wasting (SW) and simple virilizing (SV). Sanger sequencing combined with multiplex ligation-dependent probe amplification(MLPA) were used to detect the mutations of CYP21A2 gene.The patients were divided into 3 groups according to their mutations severity: severe mutation group, moderate mutation group and unknown mutation group.Then, the correlation between genotype and phenotype was analyzed. Results:(1) Forty-eight 21-OHD patients included 28 SW cases and 20 SV cases, and the first visiting age of SW was younger than that of SV, and the difference was statistically significant ( U=44.5, P<0.05). The SW cases had high incidence rate of adrenal crisis and the SV patients were liable to advanced bone age and precocious puberty.(2) Forty-four patients were detected abnormal gene mutation and the positive rate of genetic diagnosis was 91.7%.Fourteen mutation types including I2G, Del, I173N, R357W, R484fs(c.1451_1452delGGinsC, c.1450dupC), R483fs, G111Vfs*21, Q319X, c.292+ 1G>A, c.377C>G, E6Cluster, p.H393Q and m. 1647C>T, were found in 88 alleles.The most frequent mutations were I2G(36.4%), I173N(20.4%), and Del(22.7%). p.H393Q and m. 1647C>T were 2 novel mutations.I2G (47.3%) and Del (27.3%) were the most frequent mutations in SW cases, and I173N (48.5%) was the most frequent mutation in SV cases.(3) Severe mutation was in 29 patients, including 26 SW, and moderate mutation was in 13 patients, including 12 SW.The percentage of SW in severe mutation group was 89.7% and SV in moderate mutation was 92.3%. Conclusions:I2G, I173N and Del were the frequent mutations of 21-OHD in Hunan, and the total percen-tage was 79.5%.Genotype of 21-OHD has strong correlation with clinical phenotype, which can effectively predict SW by severe mutation and predict SV by moderate mutation.

OBJECTIVE To study the clinical features of children with adenovirus pneumonia and hemophagocytic lymphohistiocytosis (HLH). METHODS A retrospective analysis was performed on the mediacal data of 7 children with adenovirus pneumonia and HLH from March to September, 2019. RESULTS The age of these children ranged from 11 months to 5 years, and among these children, 5 were aged <2 years and 5 were boys. None of these children had underlying diseases. All children were hospitalized due to persistent high fever and cough, and the peak temperature of fever was 39°C to 41°C. With disease progression, 7 children developed hepatomegaly and 6 developed splenomegaly. Routine blood test results showed reductions in two or three lineages of blood cells, with increases in serum ferritin (SF), C-reactive protein (CRP), procalcitonin (PCT), and lactate dehydrogenase (LDH). Phagocytosis of blood cells was observed in 6 children. Radiological examination of lungs showed pneumonia changes. All 7 children were diagnosed with human adenovirus type 7 infection based on pathogenic metagenome detection. No abnormality was found by HLH gene detection and the children were diagnosed with secondary HLH. All children received intravenous immunoglobulin. Among these children, 4 received dexamethasone and etoposide chemotherapy, 3 received dexamethasone alone, and 4 received plasma exchange. Of the 7 children, 2 died and 5 were recovered. Compared with those who survived, the children who died had significantly greater reductions in the three lineages of blood cells and significantly greater increases in serum levels of CRP, PCT, SF, and LDH. CONCLUSIONS The children with adenovirus pneumonia and HLH have main clinical features of persistent high fever, progressive reductions in two or three lineages of peripheral blood cells, and involvement of other organ systems, including hepatosplenomegaly. Significant increases in serum levels of CRP, PCT, SF, and LDH may suggest a poor prognosis.

Background: Nonalcoholic fatty liver disease (NAFLD) is a severe liver disease, which influences the health of people worldwide. However, the specific mechanism of the disease remains unknown, and effective treatments are still lacking. It was reported that Nuclear enriched abundant transcript 1 (NEAT1) obviously was up-regulated in NAFLD model. But the role and underlying mechanism of NEAT1 in NAFLD is unclear. Methods: HepG2 cells were treated by free fatty acids (FFA) and C57BL/6J mice were treated by high-fat diet to establish NAFLD in vitro and in vivo models, respectively. Cell transfection was applied to regulate the expression of NEAT1, ROCK1, and miR-146a-5p. Western blotting and qRT-PCR were used for measuring expression of protein and mRNA level, respectively. Dual luciferase assay was used to detect the target relationship. Oil Red O staining was used to measure the lipid accumulation. HE staining was used for observing pathological feature of liver tissues. Results: High levels of NEAT1 and ROCK1, and low level of miR-146a-5p were identified in NAFLD models. NEAT1 could target miR-146a-5p to promote ROCK1 expression. Knockdown of NEAT1, overexpression of miR-146a-5p and knockdown of ROCK1 inhibited lipid accumulation through activating AMPK pathway. Conclusion: NEAT1 may regulate NAFLD through miR-146a-5p targeting ROCK1, and further affect AMPK/SREBP pathway. This study may provide a new thought for the treatment of NAFLD.

特发性矮小症(idiopathic short stature,ISS)是一种常见的儿科疾病,发病率高达 60％ 以上,且逐年上升 [1].它是指患儿的性别及机体生长激素水平等指标均正常的前提下,其身材比正常同龄儿童矮小,且未伴有进行性和病理性变化.此外,特发性矮小症患儿在自信心、认知能力、社交能力等均存在不同程度的问题,若未给予及时有效的治疗,不利于患儿的成长.目前,随着对特发性矮小症研究的深入,治疗方法种类也随之增加,如营养支持疗法、药物疗法、饮食治疗等,其中药物疗法的效果最显著.重组人生长激素(recombinant human growth hormone,rhGH)作为一种新型特发性矮小症治疗药物,可以显著促进蛋白质合成、骨骼生长,从而改善身材矮小的症状,且不会引起过度发育 [2].鉴于此,本研究观察了 rhGH 联合营养支持治疗特发性矮小症患儿的疗效,并分析其对患儿胰岛素样生长因子水平的影响,现报道如下.

This paper reports the clinical and genetic characteristics of a case of combined pituitary hormone deficiency type I (CPHD1) caused by POU domain, class 1, transcription factor 1 (POU1F1) gene variation. A 2 years and 3 months old girl mainly presented with short stature, special facial features of prominent forehead, enophthalmos, and short mandible, loose skin, central hypothyroidism, complete growth hormone deficiency, and anterior pituitary hypoplasia. Gene analysis identified a novel heterozygous mutation, c.889C>T (p.R297W), in POU1F1 gene, and this locus of her parents was wild-type. This mutation was analyzed as a possible pathogenic variant according to the guidelines of the American College of Medical Genetics and Genomics, which has not been previously reported in the literature and conforms to the autosomal dominant inheritance. This child was diagnosed with CPHD1. Her height increased by 19.8 cm and showed a catch-up growth trend after one year of combined treatment with growth hormone and euthyrox. This study enriches the mutation spectrum of POU1F1 gene and has important significance for the diagnosis and classification of combined pituitary hormone deficiency.

Objective:To explore the effects of Qinyu Sanlong decoction on expression of secreted frizzled-related proteins (SFRP)-2 antagonistic Wnt signal pathway.Method:Based on the previous research,LLC cells were used to construct lung cancer model.The mice bearing tumor were divided into model group (M),Qinyu Sanlong decoction groups (low,middle and high dose groups,named as QL,QM,QH respectively),chemotherapy group (C),and combination group (CQH).Qinyu Sanlong decoction groups were administrated with 20.12,40.24,and 80.48 g·kg-1·d-1 by gavage.C group was given with 0.4 mL cisplatin by intraperitoneal injecting.CQH group was administered with high dosage of Qinyu Sanlong decoction by gavage and cisplatin by intraperitoneal injecting.M group was administered with the same amount of 0.9％ sodium chloride solution,once a day for 21 d.The tumors were weighed to calculate the tumor inhibition rate.Transmission electron microscopy was used to observe the ultrastructure of tumor.The SFRP-2 andβ3-catenin protein expression levels in tumor tissues were detected by Western blot.Result:As compared with M group,every medication group could down-regulate β-catenin expression (P ＜0.01);as compared with QL group,other medication groups also could down-regulate β-catenin expression (P ＜ 0.01);as compared with C group,the down-regulation was more obvious in QM group,QH group and CQH group (P ＜0.05,P ＜0.01).The results of SFRP-2 showed that SFRP-2 expression was upregulated in QM and QH groups as compared with M group (P ＜ 0.05,P ＜ 0.01);every other medication group also could up-regulate SFRP-2 expression as compared with QL group (P ＜ 0.01);QM and QH groups could upregulate SFRP-2 expression as compared with C group (P ＜ 0.05,P ＜ 0.01).Also,apoptosis was found under electron microscope in medication groups,especially in QH,C and CQH groups.Conclusion:Qinyu Sanlong decoction can effectively inhibit tumor growth,induce apoptosis,promote the SFRP-2 expression and inhibit the Wnt/β-catenin signal pathway.

Lung cancer is one of the most fatal cancers due to its high metastatic rate. Traditional Chinese medicine has been used in cancer patients for decades to improve quality of life and prolong survival time. The present study used a novel Qiyusanlong (QYSL) decoction composed of 10 kinds of Chinese medicine including astragalus membranaceus (Huangqi), polygonatumod oratum (yuzu), scolopendra (tianlong), pberetima (dilong), solanum nigrum (longkui), herbahedyotis (baihushecao), semen coicis (yiyiren), euphorbia helioscopia (zeqi), curcuma longa (eshu) and tendril-leaved fritillary bulb (chuanbei). The effects and function of the QYSL decoction remain to be elucidated. The present study established a mouse xenograft model using Lewis lung carcinoma cell injection and administered different doses of QYSL decoction to the mice. It was demonstrated that the chemotherapy drug Cisplatin (DDP) and QYSL decoction repressed lung tumor growth, and the inhibitory effect of DDP was more significant. Furthermore, QYSL decoction and DDP modulated the expression of regulatory proteins in the Wnt/β‑catenin pathway, including Wnt1, Wnt2, Wnt5a and glycogen synthase kinase 3β, detected by western blotting, and affected the signals of cluster of differentiation 44 variation 6 and Survivin in tumor tissues, examined via immunohistochemistry. The combination of QYSL decoction and DDP enhanced the inhibitory effect. These data demonstrated that the QYSL decoction repressed lung tumor development via the Wnt/β‑catenin pathway. The therapeutic effect of QYSL decoction alone was milder compared with DDP, however the combination of QYSL decoction and chemotherapy exhibited an increased the rapeutic effect compared with the treatments administered alone. These findings revealed the function of QYSL decoction as a lung cancer treatment and provided insight for a novel lung cancer therapy.

目的 观察芪玉三龙汤对肺癌荷瘤小鼠瘤体的抑瘤效应及对Wnt/β-连环蛋白(Wnt/β-catenin)信号通路中糖原合成酶激酶3β(GSK3β)、磷酸化GSK3β(p-GSK3β)、β-catenin蛋白表达的影响.方法 采用Lewis肺癌细胞株培养移植法建立肺癌荷瘤小鼠模型,按随机数字表法分为模型组、化疗组和芪玉三龙汤低、中、高剂量组以及联合组,每组8只.制模第2天开始,芪玉三龙汤低、中、高剂量组小鼠分别按20.12、40.24、80.48 g·kg-1·d-1灌胃中药,化疗组每周腹腔注射0.4 mL顺铂,联合组给予高剂量中药灌胃和顺铂腹腔注射联合用药,模型组给予等量生理盐水,连续给药21 d.实验结束后处死小鼠取肺组织,称取瘤质量,计算抑瘤率;用蛋白质免疫印迹试验(Western Blot)检测肿瘤组织GSK3β、p-GSK3β、β-catenin的蛋白表达水平.结果 与模型组比较,各药物组瘤质量、GSK3β、β-catenin的蛋白表达水平均明显降低,抑瘤率、p-GSK3β的蛋白表达水平明显升高,联合组瘤质量、抑瘤率的变化较芪玉三龙汤低、中、高剂量组更显著 〔瘤质量(g):1.48±0.71比4.53±1.34、4.27±0.62、3.45±1.05,抑瘤率:73.23％比13.51％、18.32％、33.86％,均P<0.01〕,联合组瘤质量、抑瘤率与化疗组相当〔瘤质量(g):1.48±0.71比1.49±0.68,抑瘤率:73.23％比73.01％,均P>0.05〕;而联合组GSK3β、p-GSK3β的蛋白表达水平变化也较芪玉三龙汤低、中、高剂量组和化疗组更显著〔GSK3β/β-肌动蛋白(β-actin):0.58±0.03比1.02±0.02、1.06±0.04、0.96±0.04、0.78±0.05,p-GSK3β/β-actin:1.93±0.05比1.40±0.09、1.41±0.06、1.60±0.06、1.79±0.02,均P<0.05〕,但对β-catenin蛋白表达的影响以芪玉三龙汤高剂量组的降低程度较化疗组和芪玉三龙汤低中剂量组及联合组更显著(β-catenin/β-actin:0.16±0.01比0.80±0.05、1.33±0.04、0.74±0.05、0.73±0.02).结论 芪玉三龙汤对肺癌移植瘤具有温和的抑制作用,高剂量抑制肿瘤生长作用较优,且量效关系明显.芪玉三龙汤和化疗药联用具有协同效应,对肺癌具有一定的抑制作用.