ObjectiveTo observe the effect of Yifei Jianpi prescription on the of signal transducer and activator of transcription protein 1 （STAT1）/interferon regulatory factor 3 （IRF3） signaling pathway in a pneumonia model induced by lipopolysaccharide （LPS） and to explore the mechanism of Yifei Jianpi prescription in improving lung immune and inflammatory responses. MethodsSixty male SPF SD rats were used in this study. Ten rats were randomly assigned to the normal control group， and the remaining 50 were instilled with LPS in the trachea to establish a pneumonia model. After successful modeling， the rats were randomly divided into the model group， dexamethasone group （0.5 mg·kg^-1）， and Yifei Jianpi prescription high-dose （12 mg·kg^-1）， medium-dose （6 mg·kg^-1）， and low-dose （3 mg·kg^-1） groups， with 10 rats in each group. Treatment was administered once daily， and the normal control and model groups received the same volume of normal saline. After 14 days， flow cytometry was used to detect the classification of whole blood lymphocytes. Enzyme-linked immunosorbent assay （ELISA） was used to measure serum levels of immunoglobulin G （IgG）， immunoglobulin A （IgA）， immunoglobulin M （IgM）， and the content of tumor necrosis factor-α （TNF-α）， interleukin-8 （IL-8）， interleukin-6 （IL-6）， and interleukin-10 （IL-10） in alveolar lavage fluid （BALF）. Hematoxylin-eosin （HE） staining was used to observe lung tissue pathology and score the damage. Thymus weight， spleen weight， and wet-to-dry weight ratio （W/D） were recorded. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of STAT1， IRF3， IL-6， and interferon-alpha （IFN-α） in lung tissues， while Western blot was performed to assess the protein expression of STAT1， IRF3， IL-6， and IFN-α. ResultsCompared with the normal control group， the model group showed significantly increased proportion of B lymphocytes in peripheral blood， decreased proportions of NK cells and CD4⁺/CD8⁺ （P<0.05， P<0.01）， decreased serum levels of IgG and IgA， significantly increased IgM levels （P<0.01）， significantly elevated content of TNF-α， IL-6， and IL-8 in BALF， and significantly decreased IL-10 levels （P<0.01）. Lung tissue damage was evident， with significant increases in thymus and spleen weights and a higher W/D ratio （P<0.01）. The mRNA and protein expression of STAT1， IRF3， IFN-α， and IL-6 in lung tissues was significantly upregulated （P<0.05，P<0.01）. Compared with the model group， the Yifei Jianpi prescription groups showed significantly reduced proportions of B lymphocytes in peripheral blood， increased proportions of NK cells and CD4⁺/CD8⁺ ratios （P<0.05， P<0.01）， significantly increased serum levels of IgG and IgA， significantly decreased IgM levels （P<0.05， P<0.01）， significantly reduced levels of TNF-α， IL-6， and IL-8 in BALF， and significantly increased IL-10 levels （P<0.01）. Lung tissue damage was alleviated， thymus and spleen weights were significantly reduced， and the W/D ratio was markedly decreased （P<0.01）. The mRNA and protein expression of STAT1， IRF3， IFN-α， and IL-6 in lung tissues was significantly downregulated （P<0.05， P<0.01）. ConclusionYifei Jianpi prescription can alleviate lung tissue damage and improve immune and inflammatory responses in LPS-induced pneumonia rats. The mechanism may be related to the inhibition of STAT1/IRF3 signaling pathway activation.

Objective:To explore the possible risks of re-fracture after bone healing in children with congenital pseudarthrosis of the tibia, who were treated with combined surgery.Methods:56 children (35 males and 21 females, with an average age of 38.0±9.2 months ranging from 18 to 66 months) with re-fracture after bone healing were retrospectively enrolled from January 2007 to August 2016, during which a total of 142 children with CPT underwent combined surgical treatment in the orthopedics department of Hunan Children's Hospital. Complete healing of the tibial pseudarthrosis, trauma after surgery, breakage of fibula, and the distal end of the tibial intramedullary rod located in the tibial medullary cavity or not were hypothesized as 4 risk factors. Univariate logistic regression analysis was conducted to investigate the correlation between these factors and re-fractures after tibial pseudarthrosis healing.Results:The average follow-up was 81.7±10.8 months ranging from 60 to 120 months with at least 5 years after bone healing. For complete or partial healing of the tibial pseudarthrosis after surgery, the number of re-fractures was 48 and 8, respectively; For with or without a history of trauma, the number of re-fractures was 50 and 6, respectively; for with an intact or broken fibula after surgery, the number of re-fractures was 7 and 49, respectively; For entry or no entry of the intramedullary rod into the tibial medullary cavity, the number of re-fractures was 44 and 12, respectively. The results of univariate logistic regression analysis showed that partial healing of the tibial pseudarthrosis after surgery [ OR=0.255, 95% CI (0.107, 0.605), P=0.002], history of trauma [ OR=36.458, 95% CI (13.332, 99.701), P<0.001], incomplete fibula [ OR=0.267, 95% CI (0.108, 0.661), P=0.004], and intramedullary rod insertion into the tibial medullary cavity [ OR=2.640, 95% CI (1.224, 5.695), P=0.013] were associated with re-fracture after bone healing. The number and proportion of cases with recurrent fractures occurring ≤1, 1-3, 3-6, ≥6 years after bone healing were 5 cases, 9% (5/56), 14 cases, 25% (14/56), 22 cases, 39% (22/56), 15 cases, and 27% (15/56), respectively, the difference was statistically significant (χ 2=11.569, P=0.009). With the extension of follow-up time, the number of cases of re-fractures after bone healing increases, mostly occurring more than one year after bone healing. There were 44 cases (47%, 44/94) and 12 cases (25%, 12/48) of re fractures after bone healing in 94 cases of distal intramedullary rods in the tibial medullary cavity and 48 cases of cross ankle joint fixation, respectively. The difference in the incidence of re-fractures was statistically significant (χ 2=6.327, P=0.018). The incidence of intramedullary rod displacement in cases where the distal end of the intramedullary rod is located within the tibial medullary cavity was 100%. Conclusions:Factors of partial healing of the tibial pseudarthrosis, a history of trauma, incomplete status of the fibula after surgery, and intramedullary rod's entry into the tibia were risk factors for re-fracture after bone healing treated with combined surgery for CPT. After the healing of the tibial pseudarthrosis, it is not advisable to push the tibial intramedullary rod into the tibial medullary cavity, which can cause unstable fixation of the tibial intramedullary rod and result in displacement, and even affect the development of the tibial mechanical axis or the occurrence of re-fractures.

Objective To observe splenic T cell apoptosis and XIAP-associated factor 1(XAF1),FAS,and tumor necrosis factor(TNF)-α protein expression levels in rats with acute lung injury(ALI),and to determine their roles in the protective effect of Yifei Jianpi formula.Methods Sixty male specific pathogen-free SD rats were divided randomly into blank,model,positive control,and high-,medium-,and low-dose Yifei Jianpi formula groups.Rats in the positive control group were given 0.5 g/kg dexamethasone by gavage,and rats in the high-,medium-,and low-dose Yifei Jianpi formula groups were given 12,6,and 3 g/kg Yifei Jianpi formula by gavage,respectively.Rats in the model and blank groups were given equal amounts of saline by gavage.All medications were administered once a day for 14 days.Lung function testing was carried out in all rats.We observed the imaging characteristics of the lungs and changes in the organ index and lung tissue wet/dry weight(W/D)in each group,and detected the pathological changes in lung tissues by hematoxylin-eosin staining.Splenic T-cell subpopulations(CD4+/CD8+)and apoptosis of splenic T-cells were detected by flow cytometry and XAF1,FAS,and TNF-α protein expression levels in the spleen were detected by Western Blot.Results Rats in the model group showed reduced lung function,decreased spleen and thymus organ indexes,and significantly higher W/D of lung tissue(P＜0.01).In addition,they had inflammatory exudation and alveolar rupture in the lung tissue,accompanied by thickening of the lung texture and large areas of ground-glass shadows,with a significant decrease in T-cell subsets(CD4+/CD8+)and significant increases in XAF1,FAS,and TNF-α proteins,and in the rate of T-cell apoptosis(P＜0.01).Yifei Jianpi formula significantly reduced the W/D spleen of rat lung tissues,significantly increased the thymus organ index(P＜0.05,P＜0.01)and the T-cell subpopulation(CD4+/CD8+),and significantly decreased the protein expression levels of XAF1,FAS,and TNF-α,and the T-cell apoptosis rate(P＜0.05,P＜0.01).Conclusions ALI induced up-regulation of XAF1,FAS,and TNF-α protein expression and T-cell apoptosis in the spleen of rats,and Yifei Jianpi formula may protect against ALI by down-regulating these factors.

Pulmonary fibrosis is a respiratory system disorder characterized by damage to alveolar epithelial cells,pathological proliferation and transformation of fibroblasts,excessive deposition of extracellular matrix,leading to structural damage and loss of function in lung tissues,with a high mortality rate and limited effective treatment methods.This article was based on the TCM understanding of"lung connecting to large intestine",namely the theory of"lung and the large intestine being interior-exterior related",and set the modern medical understanding of"lung connecting to large intestine",namely the theory of"gut-lung axis"as the key.Combining the TCM pathogenesis of pulmonary fibrosis and the related mechanisms of"gut-lung axis"in pulmonary fibrosis,it preliminarily expounded the connotation of TCM regulating the"gut-lung axis"to treat pulmonary fibrosis,aiming to provide new ideas for clinical treatment of pulmonary fibrosis through the"gut-lung axis".

ObjectiveTo observe the effect of Banxia Xiexintang containing intestinal absorption solution （BXCIAS） on migration and invasion of polymorphonuclear myeloid-derived suppressor cells （PMN-MDSCs） in gastric cancer microenvironment. MethodThe complex solution （containing 0.63 g·mL^-1 crude drug） was prepared. Gastric cancer cells were subjected to non-contact co-culture with PMN-MDSCs in Transwell chamber to create gastric cancer microenvironment. Cell counting kit-8 （CCK-8） assay was used to screen the optimal intervention concentration and time of BXCIAS on PMN-MDSCs for subsequent experiment. The blank group， model group， FAK inhibitor group， and BXCIAS groups （26%， 18%， and 10%） were designed. Scratch assay and Transwell assay were employed to detect the migration and invasion ability of PMN-MDSCs， and enzyme-linked immunosorbent assay （ELISA） to measure the expression of vascular endothelial cell growth factor （VEGF） and matrix metalloproteinase-9 （MMP-9） in tumor microenvironment. The expression levels of PMN-MDSCs pathway-related proteins FAK， phosphorylated （p）-FAK， protein tyrosine kinase （Src）， and p-Src were detected by Western blot. ResultThe inhibition rates of PMN-MDSCs by 5%， 50%， 75%， and 100% BXCIAS at 48 h were higher than those at 24 h （P<0.05， P<0.01）. The inhibition rate of PMN-MDSCs by 50% BXCIAS at 72 h was lower than that at 48 h （P<0.01）， and the inhibition rates by 5% and 100% BXCIAS at 72 h were higher than those at 48 h （P<0.05， P<0.01）. There was no significant difference in the inhibition rate by other concentration levels at 48 h. The half-maximal inhibitory concentration （IC₅₀） at 48 h was 18.09%， indicating that 18% BXCIAS and 48 h were the optimal concentration and time， respectively. The migration distance of PMN-MDSCs was large （P<0.01）， and the number of migrating and invading cells increased （P<0.01） in the mode group compared with those in the blank group. Compared with model group， FAK inhibitor and BXCIAS at different concentration decreased the migration distance of PMN-MDSCs （P<0.01）， and the number of migrating and invading cells （P<0.01）， especially the 26% BXCIAS （P<0.01）. The expression of PMN-MDSCs pathway-related proteins FAK， p-FAK， Src and p-Src （P<0.01） and the expression of VEGF and MMP-9 （P<0.01） were higher in the model group than in the blank group. Compared with model group， FAK inhibitor and BXCIAS （26%， 18%， 10%） decreased the expression of FAK， p-FAK， and Src （P<0.01）， and FAK inhibitor and 18% BXCIAS reduced the expression of p-Src （P<0.01）， and the expression of VEGF and MMP-9 （P<0.01）. ConclusionBXCIAS can inhibit the migration and invasion of PMN-MDSCs by down-regulating the expression of FAK， p-FAK， Src， and p-Src proteins in the FAK signaling pathway of PMN-MDSCs in gastric cancer microenvironment.

ObjectiveTo observe the effect of Banxia Xiexintang （BXT）-containing intestinal absorption solution on the apoptosis of polymorphonuclear myeloid-derived suppressor cells （PMN-MDSCs） in gastric cancer microenvironment. MethodBXT-containing intestinal absorption solution was prepared， and gastric cancer cells and PMN-MDSCs were non-contact co-cultured in Transwell chamber to establish gastric cancer microenvironment. Cell counting kit-8 （CCK-8） assay was used to screen the optimal intervention concentration and time of 0-100% BXT-containing intestinal absorption solution prepared by 0.63 g·mL^-1 reconstitution solution. Cells were classified into blank group， model group， oxaliplatin group （10 mg·L^-1）， and BXT （26%， 18%， 10% BXT-containing intestinal absorption solution） group， and the apoptosis of PMN-MDSCs was detected by flow cytometry. The expression of apoptosis-related B-cell lymphoma 2 （Bcl-2）， Bcl-2-associated X protein （Bax）， and cysteine-aspartic acid protease-3 （Caspase-3） in PMN-MDSCs was detected by Western blot. ResultAfter treatment for 24 h and 48 h， the PMN-MDSCs-inhibiting rate was increased by 5%， 50%， 75%， and 100% BXT-containing intestinal absorption solution compared with that in the blank group （P<0.05， P<0.01）. At 72 h， the PMN-MDSCs-inhibiting rate by 50% BXT-containing intestinal absorption solution was lower than that at 48 h （P<0.01）， and the PMN-MDSCs-inhibiting rate by 5%， 75%， and 100% BXT-containing intestinal absorption solution showed no significant difference from that at 48 h. Moreover， the half-maximal inhibitory concentration （IC₅₀） at 48 h was 18.40%. Thus， 18% BXT-containing intestinal absorption solution and 48 h were the optimal intervention concentration and time. The survival rate of PMN-MDSCs in model group was higher than that in the blank group （P<0.05）， and the apoptosis rate was lower than that in the blank group （P<0.05）. Compared with model group， BXT containing intestinal absorption solution lowered the survival rate and raised apoptosis rate of PMN-MDSCs （P<0.05）， particularly the 26% BXT-containing intestinal absorption solution （P<0.05）. The expression of Bax and Caspase-3 in PMN-MDSCs was lower in the model group than in the blank group （P<0.05）， and the expression of Bcl-2 was higher in the model group than in the blank group （P<0.05）. The expression of Caspase-3 in PMN-MDSCs increased （P<0.05） and the expression of Bcl-2 decreased （P<0.05） in oxaliplatin group and BXT group compared with those in the model group. The expression of Bax rose in oxaliplatin group and BXT group （10% BXT-containing intestinal absorption solution） （P<0.05）. ConclusionBXT can induce the apoptosis of PMN-MDSCs by regulating the expression of apoptosis-related proteins Bax， Caspase-3， and Bcl-2 in gastric cancer microenvironment.

Gastric cancer （GC） is one of the common malignant tumors， and the incidence and mortality of GC in China rank first in the world. At present， the pathogenesis of GC has not been fully clarified. Although surgery， radiotherapy， chemotherapy， targeted therapy， and immunotherapy have achieved good results in the treatment of GC， there are still many complications， decreased sensitivity， and severe side effects. Banxia Xiexintang， derived from Treatise on Cold Damage and Miscellaneous Diseases（《伤寒杂病论》）， has been clinically used for more than 2000 years with the effects of combining cold and warm drugs， dissipating mass， and relieving stuffiness， and is a classic prescription for treating digestive tract diseases in later generations. Through clinical observation and experimental research， it is found that Banxia Xiexintang and its single drugs have good effect in preventing and treating GC. Chinese medicine has multi-component and multi-target characteristics and can treat GC through various mechanisms. Therefore， it is necessary to carry out systematic and in-depth research from the aspects of molecular biology and network pharmacology， and comprehensively reveal the mechanism of Banxia Xiexintang in preventing and treating GC. At present， the mechanism of Banxia Xiexintang in treating GC mainly focuses on inducing apoptosis of GC cells， inhibiting proliferation， migration， and invasion of GC cells， protecting peritoneal mesothelial cells， inhibiting peritoneal metastasis of GC cells， regulating GC microenvironment， and inhibiting the malignant transformation of bone marrow mesenchymal stem cells （BMSCs）. This research group is committed to the prevention and treatment of GC with Banxia Xiexintang， aiming to comprehensively reveal the mechanism of action and the pharmacodynamic material basis of Banxia Xiexintang in the prevention and treatment of GC， and provide an important scientific basis for further clinical application of Banxia Xiexintang. After searching CNKI， PubMed， Wanfang Data， VIP， and other databases， this paper summarized Banxia Xiexintang in the treatment of GC from the aspects of prescription basis， material basis， network pharmacology， clinical and experimental studies， etc.， so as to provide references for further research on pharmacological effect of Banxia Xiexintang and its application in the clinical treatment of GC.

Objective:To investigate the efficacy of phenolamine in the treatment of sepsis-induced myocardial dysfunction and its effect on cardiac function, myocardial injury index, and hemodynamics in patients.Methods:The clinical data of 79 patients with sepsis-induced myocardial dysfunction who received treatment in Huangshi Central Hospital, Edong Healthcare Group from February 2017 to February 2020 were retrospectively analyzed. These patients were divided into a control group (without phenolamine treatment, n = 41) and an observation group (with phenolamine treatment, n = 38) according to whether they received phenolamine treatment or not. Clinical efficacy, cardiac function, myocardial injury index, and hemodynamic index pre- and post-treatment were compared between the two groups. Results:There was no significant difference in 28-day mortality rate between the two groups ( P > 0.05). Intensive care unit length of stay and mechanical ventilation duration in the observation group were (9.33 ± 3.52) days and 83.00 (28.50, 138.00) hours, which were significantly shorter than (12.17 ± 4.15) days and 111.00 (47.50, 169.00) hours in the control group ( t = 3.26, Z = -2.27, both P < 0.05). The response rate in the observation group was significantly higher than that in the control group [81.58% (31/38) vs. 60.98% (25/41), χ2 = 4.05, P < 0.05]. After 7 days of treatment, the left ventricular ejection fraction in each group was significantly increased, and the left ventricular end-diastolic diameter and left ventricular end-systolic diameter in each group were significantly decreased compared with before treatment (all P < 0.05). After 7 days of treatment, the left ventricular ejection fraction in the observation group was significantly higher than that in the control group ( t = 3.29, P < 0.05), and left ventricular end-diastolic diameter and left ventricular end-systolic diameter were significantly lower than those in the control group ( t = 5.94, 11.21, both P < 0.05). N-terminal pro-brain natriuretic peptide and cardiac troponin I levels in each group were significantly decreased with time (both P < 0.05). At 24 and 72 hours and 7 days after treatment, N-terminal pro-brain natriuretic peptide and cardiac troponin I levels in the observation group were significantly lower than those in the control group (both P < 0.05). After 7 days of treatment, heart rate in each group decreased significantly compared with that before treatment (both P < 0.05), mean arterial pressure, cardiac index, and stroke output index in each group increased significantly compared with those before treatment (all P < 0.05). After 7 days of treatment, heart rate in the observation group was significantly lower than that in the control group ( t = 4.90, P < 0.05), and mean arterial pressure, cardiac index, and stroke output index in the observation group were significantly higher than those in the control group ( t = 4.37, 3.23, 6.01, all P < 0.05). Conclusion:Phentolamine can improve hemodynamics, reduce myocardial injury and improve cardiac function in patients with sepsis-induced myocardial dysfunction.

Objective:To analyze blood transfusion and prognostic factors of extracorporeal membrane pulmonary oxygenation (ECMO) for the treatment of respiratory and circulatory failure.Methods:The clinical data of 80 patients with respiratory and circulatory failure who received treatment in Huangshi Central Hospital from March 2016 to July 2021 were retrospectively analyzed. According to 28-day prognosis, these patients were divided into death group ( n = 44) and survival group ( n = 36). The general data, blood transfusion during the process of ECMO, vital signs, laboratory indicators, ventilation time, and length of hospital stay were compared between the two groups. The factors affecting death during the process of ECMO were analyzed. Results:There were no significant differences in sex, age, body mass index, complications, the cause of respiratory and circulatory failure, and the mode of ECMO between the two groups (all P > 0.05). Preoperative Acute Physiology and Chronic Health Evaluation II score, creatinine, procalcitonin and lactic acid levels in the survival group were (22.36 ± 3.71) points, (79.17 ± 9.29) μmol/L, (2.77 ± 0.79) ng/L, (2.74 ± 0.36) mmol/L, respectively, which were significantly lower than (34.27 ± 4.98) points, (94.16 ± 10.23) μmol/L, (3.69 ± 1.10) ng/L, (5.18 ± 0.42) mmol/L, respectively in the death group ( t = -11.89, -6.79, -5.62, -27.53, all P < 0.001). There were no significant differences in preoperative respiratory frequency, diastolic pressure, systolic pressure, heart rate, oxygenation index (PaO 2/FiO 2) and C-reactive protein between the two groups (all P > 0.05). The volume of blood transfused on the day of undergoing ECMO, the volume of blood transfused on the day of withdrawing ECMO, the volume of blood transfused during the whole process of ECMO, duration of ventilation, and the incidence of complications related to ECMO were(98.74 ± 16.28) mL, (37.23 ± 10.36) mL, (398.79 ± 67.81) mL, (210.39 ± 20.21) hours, 38.89% (14/36), respectively, which were significantly lower than (160.17 ± 23.14) mL, (48.26 ± 12.25) mL, (600.23 ± 70.12) mL, (320.14 ± 18.21) hours, 79.55% (35/44), respectively in the death group ( t = -13.43, -4.29, 4.94, 25.25, χ2 = 13.79, all P < 0.001). The length of hospital stay in the survival group was longer than that in the death group [(20.14 ± 5.36) days vs. (14.17 ± 4.23) days, t = 5.56, P < 0.001). Acute Physiology and Chronic Health Evaluation II score, procalcition level, the volume of blood transfused on the day of ECMO, duration of ventilation, and the volume of blood transfused during the whole process of ECMO are risk factors for death after ECMO, while length of hospital stay is a protective factor for ECMO. Conclusion:Preoperative evaluation of Acute Physiology and Chronic Health Evaluation II score, continuous blood transfusion during the whole process of ECMO, grasping the opportunity of ventilation and preventing against complications of ECMO are the keys to increasing the survival rate of patients with respiratory and circulatory failure.

Objective:To investigate the role of long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) in the resistance of pancreatic cancer PANC1 cells to gemcitabine (GEM), and clarify the relationship between SNHG1 and miR-330.Methods:The clinical data of 179 pancreatic tissue samples and 171 adjacent normal pancreas tissues were collected from the Cancer Genome Atlas (TCGA), and bioinformatics analysis was performed to analyze the expression of SNHG1 and miR-330 in pancreatic cancer tissue and adjacent normal tissue. PANC1 cell line with the resistance to GEM was established by the intermittent gradient doubling method in vitro. The GEM-resistant cells were divided into three groups: si-NC-GEM (negative control) group, si-SNHG1-GEM (transfected with siRNA targeting SNHG1) group, and GEM-resistant group. At the same time, to validate the role of miR-330 in targeting SNHG1 expression, the GEM-resistant cells were further divided into three groups: NC-inh+ si-NC group (co-transfected with negative control miR-330 inhibitor and si-NC), NC-inh+ si-SNHG1 group (co-transfected with negative control miR-330 inhibitor and si-SNHG1), and miR-330-inh + si-SNHG1 group (co-transfected with miR-330 inhibitor and si-SNHG1). qRT-PCR was used to detect the expression of SNHG1 and miR-330 in GEM-resistant cells. CCK-8 and immunofluorescence (Ki67) were used to test GEM-resistant cell growth and proliferation. Transwell and wound healing were used to test the migration and invasion in GEM-resistant cells. Bioinformatics analysis and luciferase reporter assay were used to verify the regulatory relationship between SNHG1 and miR-330. Results:Compared to the adjacent normal tissues of pancreatic cancer, the expression of lncRNA SNHG1 in pancreatic cancer tissues was significantly increased (6.543±0.72 vs 5.31±0.96), and the expression of miR-330 was greatly decreased (2.54±1.85 vs 3.01±1.23); and all the differences were statistically significant ( P<0.05). The expression of lncRNA SNHG1 in si-NC-GEM group, si-SNHG1-GEM group, and GEM-resistant group was 2.43±0.10, 0.26±0.08 and 3.25±0.310, which in si-SNHG1-GEM group was lower than those in si-NC-GEM group or GEM-resistant group. While the expression of miR-330 in si-NC-GEM group, si-SNHG1-GEM group, and GEM-resistant group was 0.47±0.13, 0.84±0.12 and 0.38±0.21, which in si-SNHG1-GEM group was higher than those in si-NC-GEM group or GEM-resistant group. All the differences were statistically significant ( P<0.05). Compared to the si-NC-GEM group or GEM-resistant group, A450, Ki67, number of migrated cells and the distance of invasion in si-SNHG1-GEM group were all decreased, and the differences were statistically significant ( P<0.05). Otherwise, luciferase activity of miR-330-WT in si SNHG1-GEM group was significantly higher than that in NC siRNA group (3.21±0.22 vs 1.03±0.18). The luciferase activity of SNHG1-WT in miR-330 inhibitor group was significantly lower than that in NC inhibitor group (0.97±0.21 vs 2.32±0.17). In miR-330-inh+ si-SNHG1 GEM-resistant group, the cell A450, Ki67, migration cell and distant of invasion was higher than those in NC-inh+ si-SNHG1 group, and the difference was statistically significant (all P value<0.05). Conclusions:lncRNA SNHG1 targeting miR-330 could promote GEM resistance in pancreatic cancer PANC1 cells.