Kaempferol from Alpinia officinarum Hance induces G2/M cell cycle arrest in hepatocellular carcinoma cells by regulating the ATM/CHEK2/KNL1 pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Alpinia officinarum Hance (A. officinarum), a perennial herb known for its medicinal properties, has been used to treat various ailments, such as stomach pain, abdominal pain, emesis, and digestive system cancers. A. officinarum is extensively cultivated in the Qiongzhong and Baisha regions of Hainan, and it holds substantial therapeutic value for the local Li people of Hainan. Kaempferol, a flavonoid derived from A. officinarum, has demonstrated anticancer properties in various experimental and biological studies. Nevertheless, the precise mechanisms through which it exerts its anti-hepatocellular carcinoma (HCC) effects remain to be comprehensively delineated. AIM OF THE STUDY: This investigation aims to elucidate the anti-HCC effects of kaempferol derived from A. officinarum and to delve into its underlying mechanistic pathways. MATERIALS AND METHODS: Using ultra-high performance liquid chromatography-mass spectrometry/mass spectrometry (UPLC-MS/MS) to identify active compounds in A. officinarum. HCCLM3 and Huh7 cells were used to study the anti-HCC effect of kaempferol from A. officinarum. The cytotoxicity and proliferation of kaempferol and A. officinarum were measured using CCK-8 and EDU staining. Wound-healing assays and three-dimensional tumor spheroid models were further used to evaluate migration and the anti-HCC activity of kaempferol. The cell cycle and apoptosis were evaluated by flow cytometry. Western blot and qRT-PCR were used to detect the expression of proteins and genes associated with the cell cycle checkpoints. Finally, bioinformatics was used to analyze the relationship between the differential expression of core targets in the ATM/CHEK2/KNL1 pathway and a poor prognosis in clinical HCC samples. RESULTS: UPLC-MS/MS was employed to detect five active compounds in A. officinarum, such as kaempferol. The CCK-8 and EDU assays showed that kaempferol and A. officinarum significantly inhibited the proliferation of HCC cells. A wound-healing assay revealed that kaempferol remarkably inhibited the migration of HCC cells. Kaempferol significantly suppressed the growth of tumor spheroids. In addition, kaempferol markedly induced G2/M arrest and promoted apoptosis of HCC cells. Mechanically, kaempferol significantly reduced the protein and mRNA expression levels of ATM, CHEK2, CDC25C, CDK1, CCNB1, MPS1, KNL1, and Bub1. Additionally, the combination of kaempferol and the ATM inhibitor KU55933 had a more significant anti-HCC effect. The results of bioinformatics showed that ATM, CHEK2, CDC25C, CDK1, and KNL1 were highly expressed in patients with HCC and cancer tissues, indicating that these genes have certain value in the clinical diagnosis of HCC. CONCLUSIONS: Collectively, our results revealed that kaempferol from A. officinarum inhibits the cell cycle by regulating the ATM/CHEK2/KNL1 pathway in HCC cells. In summary, our research presents an innovative supplementary strategy for HCC treatment.

Integrating network pharmacology, bioinformatics, and experimental validation to unveil the molecular targets and mechanisms of galangin for treating hepatocellular carcinoma.

BACKGROUND: Galangin, a flavonoid compound, is derived from Alpinia officinarum Hance. Previous studies have shown that galangin can inhibit the proliferation of hepatocellular carcinoma (HCC), but its mechanism is still unclear. This study aims to investigate the potential targets and molecular mechanisms of galangin on HCC through network pharmacology, bioinformatics, molecular docking, and experimental in vitro validation. METHODS: In this study, network pharmacology was used to investigate the targets and mechanisms of galangin in the treatment of HCC. AutoDockTools software was used to simulate and calculate the binding of galangin to its core targets. GO and KEGG enrichment analyses were conducted in the DAVID database to explore the main biological functions and signaling pathways impacted by galangin intervention. In addition, bioinformatics was applied to examine the correlation between the differential expressions of the anti-HCC core targets of galangin and the survival of patients with HCC. Finally, the findings obtained from network pharmacology and bioinformatics were verified in cell experiments. RESULTS: A total of 67 overlapping target genes of galangin and HCC were identified. Through the analysis of the protein-protein interaction (PPI) network, 10 hub genes with the highest degree of freedom were identified, including SRC, ESR1, MMP9, CDK4, CCNB1, MMP2, CDK2, CDK1, CHK1, and PLK1. These genes were found to be closely related to the degradation of the extracellular matrix, signal transduction, and the cell cycle. GO and KEGG enrichment analyses revealed that galangin exerts an anti-HCC role by affecting various signaling pathways, including the cell cycle, pathways in cancer, and the PI3K-Akt signaling pathway. The results of molecular docking indicated a significant interaction between galangin and CCNB1, CDK4, CDK1, and PLK1. Bioinformatics analysis revealed that CCNB1, CDK4, CDK1, and PLK1 were upregulated in the liver of patients with HCC at both the mRNA and protein levels. Flow cytometry analysis showed that galangin induced G0/G1 phase arrest and cell apoptosis in HepG2 and Huh7 cells. Additionally, galangin suppressed the expression of key proteins and mRNAs involved in the cell cycle pathway. CONCLUSIONS: These results suggest that galangin inhibits the growth of HCC cells by arresting the cell cycle at the G0/G1 phase.

Predicting maturity and identifying key factors in organic waste composting using machine learning models.

The measurement of germination index (GI) in composting is a time-consuming and laborious process. This study employed four machine learning (ML) models, namely Random Forest (RF), Artificial Neural Network (ANN), Support Vector Regression (SVR), and Decision Tree (DT), to predict GI based on key composting parameters. The prediction results showed that the coefficient of determination (R2) for RF (>0.9) and ANN (>0.9) was higher than SVR (<0.6) and DT (<0.8), suggesting that RF and ANN displayed superior predictive performance for GI. The SHapley additive exPlanations value result indicated that composting time, temperature, and pH were the important features contributing to GI. Composting time was found to have the most significant impact on GI. Overall, RF and ANN were suggested as effective tools for predicting GI in composting. This study offers the reliable approach of accurately predicting GI in composting processes, thereby enabling intelligent composting practices.

Mechanisms of Gills Response to Cadmium Exposure in Greenfin Horse-Faced Filefish (Thamnaconus septentrionalis): Oxidative Stress, Immune Response, and Energy Metabolism.

Cadmium (Cd) pollution has become a global issue due to industrial and agricultural developments. However, the molecular mechanism of Cd-induced detrimental effects and relevant signal transduction/metabolic networks are largely unknown in marine fishes. Here, greenfin horse-faced filefish (Thamnaconus septentrionalis) were exposed to 5.0 mg/L Cd up to 7 days. We applied both biochemical methods and multi-omics techniques to investigate how the gills respond to Cd exposure. Our findings revealed that Cd exposure caused the formation of reactive oxygen species (ROS), which in turn activated the MAPK and apoptotic pathways to alleviate oxidative stress and cell damage. Glycolysis, protein degradation, as well as fatty acid metabolism might assist to meet the requirements of nutrition and energy under Cd stress. We also found that long-term (7 days, "long-term" means compared to 12 and 48 h) Cd exposure caused the accumulation of succinate, which would in turn trigger an inflammatory response and start an immunological process. Moreover, ferroptosis might induce inflammation. Overall, Cd exposure caused oxidative stress, energy metabolism disturbance, and immune response in greenfin horse-faced filefish. Our conclusions can be used as references for safety risk assessment of Cd to marine economic fishes.

Complete genome analysis reveals environmental adaptability of sulfur-oxidizing bacterium Thioclava nitratireducens M1-LQ-LJL-11 and symbiotic relationship with deep-sea hydrothermal vent Chrysomallon squamiferum.

One sulfur-oxidizing bacterium Thioclava sp. M1-LQ-LJL-11 was isolated from the gill of Chrysomallon squamiferum collected from 2700 m deep hydrothermal named Longqi on the southwest Indian Ocean ridge. In order to understand its survival mechanism in hydrothermal extreme environment and symbiotic relationship with its host, the complete genome of strain M1-LQ-LJL-11 was sequenced and analyzed. A total of 6117 Mb of valid data was obtained, including 4096 coding genes, 61 non coding genes, including 9 rRNAs (among them, there are 3 in 23S rRNA, 3 in 5S rRNA, and 3 in 16S rRNA.), 52 tRNAs and 35 genomic islands. Strain M1-LQ-LJL-11 contains one chromosome and two plasmids. In the genome annotation information of the strain, we found 28 genes including cys sox, sor, sqr, tst related to sulfur metabolism and 17 metal resistance genes. Interestingly, a pair of quorum sensing system which probably regulating biofilm formation located in chromosome was found. These genes are critical for self-adaptation against severe environment as well as host survival. This study provides a basis understanding for the adaptive strategies of deep-sea hydrothermal bacteria and symbiotic relationship with its host in extreme environments through gene level.

Proteomic Analyses Reveal Functional Pathways and Potential Targets in Pediatric Hydrocephalus.

INTRODUCTION: Hydrocephalus is a common pediatric disorder of cerebral spinal fluid physiology resulting in abnormal expansion of the cerebral ventricles. However, the underlying molecular mechanisms remain unknown. METHODS: We performed proteomic analyses of cerebrospinal fluid (CSF) from 7 congenital hydrocephalus and 5 arachnoid cyst patients who underwent surgical treatment. Differentially expressed proteins (DEPs) were identified by label-free Mass Spectrometry followed by differential expression analysis. The GO and GSEA enrichment analysis was performed to explore the cancer hallmark pathways and immune-related pathways affected by DEPs. Then, network analysis was applied to reveal the location of DEPs in the human protein-protein interactions (PPIs) network. Potential drugs for hydrocephalus were identified based on drug-target interaction. RESULTS: We identified 148 up-regulated proteins and 82 down-regulated proteins, which are potential biomarkers for clinical diagnosis of hydrocephalus and arachnoid cyst. Functional enrichment analysis revealed that the DEPs were significantly enriched in the cancer hallmark pathways and immunerelated pathways. In addition, network analysis uncovered that DEPs were more likely to be located in the central regions of the human PPIs network, suggesting DEPs may be proteins that play important roles in human PPIs. Finally, we calculated the overlap of drug targets and the DEPs based on drugtarget interaction to identify the potential therapeutic drugs of hydrocephalus. CONCLUSION: The comprehensive proteomic analyses provided valuable resources for investigating the molecular pathways in hydrocephalus, and uncovered potential biomarkers for clinical diagnosis and therapy.

Integrated analysis of Dendrobium nobile extract Dendrobin A against pancreatic ductal adenocarcinoma based on network pharmacology, bioinformatics, and validation experiments.

Background: Dendrobium nobile (D. nobile), a traditional Chinese medicine, has received attention as an anti-tumor drug, but its mechanism is still unclear. In this study, we applied network pharmacology, bioinformatics, and in vitro experiments to explore the effect and mechanism of Dendrobin A, the active ingredient of D. nobile, against pancreatic ductal adenocarcinoma (PDAC). Methods: The databases of SwissTargetPrediction and PharmMapper were used to obtain the potential targets of Dendrobin A, and the differentially expressed genes (DEGs) between PDAC and normal pancreatic tissues were obtained from The Cancer Genome Atlas and Genotype-Tissue Expression databases. The protein-protein interaction (PPI) network for Dendrobin A anti-PDAC targets was constructed based on the STRING database. Molecular docking was used to assess Dendrobin A anti-PDAC targets. PLAU, one of the key targets of Dendrobin A anti-PDAC, was immunohistochemically stained in clinical tissue arrays. Finally, in vitro experiments were used to validate the effects of Dendrobin A on PLAU expression and the proliferation, apoptosis, cell cycle, migration, and invasion of PDAC cells. Results: A total of 90 genes for Dendrobin A anti-PDAC were screened, and a PPI network for Dendrobin A anti-PDAC targets was constructed. Notably, a scale-free module with 19 genes in the PPI indicated that the PPI is highly credible. Among these 19 genes, PLAU was positively correlated with the cachexia status while negatively correlated with the overall survival of PDAC patients. Through molecular docking, Dendrobin A was found to bind to PLAU, and the Dendrobin A treatment led to an attenuated PLAU expression in PDAC cells. Based on clinical tissue arrays, PLAU protein was highly expressed in PDAC cells compared to normal controls, and PLAU protein levels were associated with the differentiation and lymph node metastatic status of PDAC. In vitro experiments further showed that Dendrobin A treatment significantly inhibited the proliferation, migration, and invasion, inducing apoptosis and arresting the cell cycle of PDAC cells at the G2/M phase. Conclusion: Dendrobin A, a representative active ingredient of D. nobile, can effectively fight against PDAC by targeting PLAU. Our results provide the foundation for future PDAC treatment based on D. nobile.

Myocardin-related transcription factor A, regulated by serum response factor, contributes to diabetic cardiomyopathy in mice.

AIMS: Diabetic cardiomyopathy is a significant contributor to the global pandemic of heart failure. In the present study we investigated the involvement of myocardin-related transcription factor A (MRTF-A), a transcriptional regulator, in this process. MATERIALS AND METHODS: Diabetic cardiomyopathy was induced in mice by feeding with a high-fat diet (HFD) or streptozotocin (STZ) injection. KEY FINDINGS: We report that MRTF-A was up-regulated in the hearts of mice with diabetic cardiomyopathy. MRTF-A expression was also up-regulated by treatment with palmitate in cultured cardiomyocytes in vitro. Mechanistically, serum response factor (SRF) bound to the MRTF-A gene promoter and activated MRTF-A transcription in response to pro-diabetic stimuli. Knockdown of SRF abrogated MRTF-A induction in cardiomyocytes treated with palmitate. When cardiomyocytes conditional MRTF-A knockout mice (MRTF-A CKO) and wild type (WT) mice were placed on an HFD to induce diabetic cardiomyopathy, it was found that the CKO mice and the WT mice displayed comparable metabolic parameters including body weight, blood insulin concentration, blood cholesterol concentration, and glucose tolerance. However, both systolic and diastolic cardiac function were exacerbated by MRTF-A deletion in the heart. SIGNIFICANCE: These data suggest that MRTF-A up-regulation might serve as an important compensatory mechanism to safeguard the deterioration of cardiac function during diabetic cardiomyopathy.

Protective effects of endothelial progenitor cell microvesicles carrying miR­98­5p on angiotensin II­induced rat kidney cell injury.

With the increasing number of patients with hypertensive nephropathy worldwide, it has posed a major threat to health and studies on its treatment and pathogenesis are imminent. The present study investigated the mechanism through which microRNA (miR)-98-5p in microvesicles (MVs) secreted by endothelial progenitor cells (EPCs) is involved in the repair of angiotensin II (Ang II)-induced injury of rat primary renal kidney cells (PRKs). After isolation of rat renal cortical sections, PRKs were isolated by density gradient centrifugation and identified by immunofluorescence staining. Transmission electron microscopy identifies successful separation of Mvs. An in vitro cell injury model was constructed using Ang II. The Gene Expression Omnibus was used to analyze the differentially expressed genes between diabetic rats and normal rats, and the Kyoto Encyclopedia of Genes and Genomes was used to analyze the signaling pathways involved in these differentially expressed genes. Reverse transcription-quantitative PCR was used to analyze the effect of EPC-MVs on the expression of miRNA induced by Ang II, and the levels of target genes and signaling pathway-related proteins involved were analyzed by western blot. luciferase was used to detect the targeted binding of miR-98-5p to insulin-like growth factor 1 receptor (IGF1R). Enzyme-linked immunosorbent assay was used to analyze the effect of EPC-MVs on Ang II-induced oxidative stress and inflammation levels on PRKs. Cell Counting Kit-8 was used to analyze the effect of EPC-MVs on the cell viability of PRKs induced by Ang II. The results showed that treatment of PRKs with Ang II decreased cell viability, whereas oxidative stress and inflammation were increased. However, EPC-MVs alleviated Ang II-induced damage of the PRKs. During this process, the Ang-II-induced downregulation of miR-98-5p was reversed by EPC-MVs, so miR-98-5p may be a key factor regulating the action of EPC-MVs. Dual-luciferase assay confirmed that miR-98-5p targets IGF1R. It was subsequently demonstrated that EPC-MVs overexpressing miR-98-5p promoted phosphorylation of PI3K/Akt/endothelial nitric oxide synthase (eNOS), and inhibited the oxidative stress and inflammation in PRKs, which were reversed by the overexpression of IGF1R. In conclusion, the results of the present study demonstrated that EPC-MVs with high expression of miR-98-5p can activate the PI3K/Akt/eNOS pathway by regulating IGF1R, as well as protect PRKs from Ang II-induced oxidative stress, inflammation and inhibition of cell viability.

Protective effects of endothelial progenitor cell microvesicles on Ang II­induced rat kidney cell injury.

Chronic hypertension can lead to kidney damage, known as hypertensive nephropathy or hypertensive nephrosclerosis. Further understanding of the molecular mechanisms via which hypertensive nephropathy develops is essential for effective diagnosis and treatment. The present study investigated the mechanisms by which endothelial progenitor cells (EPCs) repair primary rat kidney cells (PRKs). ELISA, Cell Counting Kit­8 and flow cytometry assays were used to analyze the effects of EPCs or EPC­MVs on the oxidative stress, inflammation, cell proliferation, apoptosis and cycle of PRKs induced by AngII. A PRK injury model was established using angiotensin II (Ang II). After Ang II induction, PRK proliferation was decreased, apoptosis was increased and the cell cycle was blocked at the G1 phase before entering the S phase. It was found that the levels of reactive oxygen species and malondialdehyde were increased, while the levels of glutathione peroxidase and superoxide dismutase were decreased. Moreover, the levels of the inflammatory cytokines IL­1ß, IL­6 and TNF­α were significantly increased. Thus, Ang II damaged PRKs by stimulating oxidative stress and promoting the inflammatory response. However, when PRKs were co­cultured with EPCs, the damage induced by Ang II was significantly reduced. The current study collected the microvesicles (MVs) secreted by EPCs and co­cultured them with Ang II­induced PRKs, and identified that EPC­MVs retained their protective effect on PRKs. In conclusion, EPCs protect PRKs from Ang II­induced damage via secreted MVs.

Hybrid Transfer Learning and Broad Learning System for Wearing Mask Detection in the COVID-19 Era.

In the era of Corona Virus Disease 2019 (COVID-19), wearing a mask can effectively protect people from infection risk and largely decrease the spread in public places, such as hospitals and airports. This brings a demand for the monitoring instruments that are required to detect people who are wearing masks. However, this is not the objective of existing face detection algorithms. In this article, we propose a two-stage approach to detect wearing masks using hybrid machine learning techniques. The first stage is designed to detect candidate wearing mask regions as many as possible, which is based on the transfer model of Faster_RCNN and InceptionV2 structure, while the second stage is designed to verify the real facial masks using a broad learning system. It is implemented by training a two-class model. Moreover, this article proposes a data set for wearing mask detection (WMD) that includes 7804 realistic images. The data set has 26403 wearing masks and covers multiple scenes, which is available at "https://github.com/BingshuCV/WMD." Experiments conducted on the data set demonstrate that the proposed approach achieves an overall accuracy of 97.32% for simple scene and an overall accuracy of 91.13% for the complex scene, outperforming the compared methods.

Local Water-Filling Algorithm for Shadow Detection and Removal of Document Images.

Shadow detection and removal is an important task for digitized document applications. It is hard for many methods to distinguish shadow from printed text due to the high darkness similarity. In this paper, we propose a local water-filling method to remove shadows by mapping a document image into a structure of topographic surface. Firstly, we design a local water-filling approach including a flooding and effusing process to estimate the shading map, which can be used to detect umbra and penumbra. Then, the umbra is enhanced using Retinex Theory. For penumbra, we propose a binarized water-filling strategy to correct illumination distortions. Moreover, we build up a dataset called optical shadow removal (OSR dataset), which includes hundreds of shadow images. Experiments performed on OSR dataset show that our method achieves an average ErrorRatio of 0.685 with a computation time of 0.265 s to process an image size of 960×544 pixels on a desktop. The proposed method can remove the shading artifacts and outperform some state-of-the-art methods, especially for the removal of shadow boundaries.

Panax japlcus var polysaccharide regulates proliferation and apoptosis of gastric cancer MKN45 cells by targeting let-7a/CDK6 molecular axis / 中国肿瘤生物治疗杂志

@#Objective: To investigate the effect of panax japlcus var polysaccharide (PJPS) on the proliferation and apoptosis of gastric cancer MKN45 cells and its regulatory mechanism. Methods: Human gastric cancer cell lines (HGC27, MGC803, MKN45) and gastric mucosal epithelial cell line GES-1 were selected for this study. Let-7a mimics and let-7a inhibitor were transfected into MKN45 cells; Gastric cancer cell lines were treated with 100 μg/ml PJPS and MKN45 was selected as the subsequent experimental cell line. MKN45 cells were cultured with 0, 10, 50, 100 and 120 μg/ml PJPS, respectively. The proliferation and apoptosis rate of MKN45 cells were detected by CCK-8 and flow cytometry, respectively. Expressions of cell cycle dependent kinase 6 (CDK6) and apoptosis-related proteins in MKN45 cells were detected by Western blotting, and the expression level of miRNAs regulating the proliferation of gastric cancer cells was detectedbyReal-timequantitativePCR(qPCR).TheDualluciferasereportergeneassaywasusedtovalidatethetargeting relationship between let-7a and CDK6. Results: Compared with other gastric cancer cells, 100 μg/ml PJPS significantly inhibited the proliferation of MKN45 cells (P<0.01). At the same time, 100 μg/ml PJPS significantly up-regulated the expression of let-7a in MKN45 cells (P<0.01). The Dual luciferase reporter gene assay confirmed that CDK6 was the target gene of let-7a. Furthermore, PJPS inhibited the expression of CDK6 by up-regulating let-7a, thereby inhibiting the proliferation and inducing apoptosis of MKN45 cells (all P<0.01). Conclusion: PJPS inhibits proliferation and induces apoptosis of gastric cancer MKN45 cells by regulating the let-7a/ CDK6 axis.

Effect of Shear Strain Rate on Microstructure and Properties of Austenitic Steel Processed by Cyclic Forward/Reverse Torsion.

In this work, commercial AISI 304 stainless steel rods were subjected to cyclic forward/reverse torsion (CFRT) treatments at low-speed and high-speed torsion at room temperature. Microstructures in the core and surface layers of the CFRT-treated samples were systematically characterized. Results show that the CFRT treatment can introduce martensite phase on the surface of the rods via strain-induced martensitic transformation. High-speed twisting is more effective in inducing martensite in the surface layer compared to low-speed twisting. During the stretching process, the overall strain-hardening behavior of the gradient material is related to the content of its gradient defects. Higher gradient martensite content results in a higher surface hardness of the material, but less overall tensile properties. The effect of twisting speed on torsion behavior and the strain-hardening mechanisms in tensile of the gradient structured steels was also addressed.

The relationship between serum hepatitis B virus DNA level and liver histology in patients with chronic HBV infection.

BACKGROUND: There is no consensus regarding the relationship between HBV DNA and liver fibrosis, and the relationship between HBV DNA and the degree of liver cirrhosis has not been reported in patients with chronic HBV infection. METHODS: From January 2011 to December 2016, liver biopsies were performed on 396 patients with chronic hepatitis B and cirrhosis. Assessments of liver fibrosis and cirrhosis were based on the Laennec staging system. RESULTS: Serum levels of HBV DNA were correlated with fibrosis and cirrhosis (KW = 73.946, P<0.001). Serum HBV DNA level was correlated with mild fibrosis, moderate to severe fibrosis and cirrhosis (P = 0.009, P<0.001, and P<0.001, respectively). The HBeAg-positive group and HBeAg-negative group showed significant differences in HBV DNA levels, and the rates of mild fibrosis, severe fibrosis and cirrhosis were significantly different between these two groups (F = 17.585, P<0.001 and F = 6.017, P = 0.003, respectively). The replication status of the serum HBV DNA affected fibrosis formation as well as cirrhosis (χ2 = 53.76, P<0.001). In the HBeAg-positive group, the sensitivity, specificity and AUC values of HBV DNA as a predictor for mild fibrosis and cirrhosis were 64.3%, 78.94% and 0.818, respectively, and 81.0%, 69.2%, and 0.871, respectively. In the HBeAg-negative group, the sensitivity, specificity and AUC values of HBV DNA for liver sclerosis prediction were 48%, 76.8% and 0.697, respectively. CONCLUSIONS: Different HBV DNA levels had different effects on the formation of fibrosis and sclerosis in liver tissues. HBV DNA levels can predict mild fibrosis and cirrhosis in liver tissue, which is enhanced in HBeAg-positive patients.

[Effect of dexmedetomidine on stress responses during extubation in patients undergoing uvulopalatopharyngoplasty].

OBJECTIVE: To observe the effect of dexmedetomidine hydrochloride on stress responses during extubation in patients undergoing uvulopalatopharyngoplasty (UPPP). METHODS: Eighty-six scheduled for UPPP under general anesthesia were randomly divided into dexmedetomidine group (group D, n = 50) and control group (group C, n = 36). All patients were transported into post anesthesia care unit (PACU) after surgery and maintained sedation and analgesia by infusing propofol and sufentanil. Patients in group D were administrated dexmedetomidine 0.5 µg/kg, group C were administrated equivalent volume of normal saline. Both groups were treated with mechanical ventilation 6 - 24 h before extubation. Recovery time, the dosage of sedative and analgesic drugs and side effects were recorded. RESULTS: There were no significant differences between two groups in recovery time (P > 0.05). The dosage of propofol and sufentanil in group D were respectively (785 ± 65) mg, (176 ± 10) µg, significantly less than that in group C (950 ± 101) mg, (209 ± 14) µg (P < 0.05). side effects in group D were significantly less than that in group C (P < 0.01). CONCLUSIONS: Dexmedetomidine hydrochloride could efficiently restrain the stress response around tracheal extubation, reduce postoperative complications in patients undergoing UPPP.