Isoliquiritigenin attenuates pathological cardiac hypertrophy via regulating AMPKα in vivo and in vitro.

Isoliquiritigenin (ISL) is a type of flavonoid, derived from the root of the legume plant Glycyrrhiza, that has multiple pharmacological properties. However, its role in cardiac remodeling induced by pressure overload has yet to be fully elucidated. Aortic banding (AB) surgery was used to establish a cardiac hypertrophy model in male C57BL/6 mice. Mice were randomly divided into four groups (n = 20 per group) as follows: Sham + vehicle, sham + ISL, AB + vehicle and AB + ISL. ISL was administered to the mice intragastrically for 1 week after the operation. To evaluate the role of ISL in mice challenged with AB, echocardiography, histological analysis and molecular biochemistry examinations were performed. ISL treatment decreased cardiac hypertrophy and improved cardiac dysfunction induced by pressure overload. In addition, ISL decreased the cross-sectional area of cardiomyocytes. Furthermore, ISL reversed the AB-mediated increase in phosphorylated (p-)mTOR and p-ERK protein levels and further increased the protein expression of p-AMP-activated protein kinase (AMPK)α in response to AB, whereas knockout of AMPKα abolished the protective effects of ISL. The present study suggested that ISL could suppress pressure overload-induced cardiac hypertrophy through the activation of AMPKα. Therefore, ISL may serve as a therapeutic target for cardiac remodeling.

Transcriptomic Analysis of Trigeminal Ganglion and Spinal Trigeminal Nucleus Caudalis in Mice with Inflammatory Temporomandibular Joint Pain.

Background: Persistent facial pain heavily impacts the quality of life in patients with temporomandibular joint (TMJ) disorders. Previous studies have demonstrated that long non-coding ribonucleic acid (lncRNA) is an important regulator of pain. In this study, we aimed to analyze lncRNA expression in the whole transcriptome of trigeminal ganglia (TG) and spinal trigeminal nucleus caudalis (Sp5C) in a chronic inflammatory TMJ pain mouse model. Methods: Chronic inflammatory TMJ pain was induced by intra-TMJ injection of complete Freund's adjuvant (CFA). Mouse TG and Sp5C tissues were harvested on day 4 after CFA injection. The lncRNA expression patterns in the whole transcriptome of TG and Sp5C were profiled with RNA sequencing. Results: We observed that 38 lncRNAs and 849 mRNAs were differentially expressed after CFA treatment. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis further revealed relationships among those differentially expressed lncRNAs and mRNAs and their potential functions. Specific categories of biological process, cellular processes, and molecular function of the differentially expressed transcripts were ascertained. Conclusion: Our results suggest that lncRNA expression in the whole transcriptome of trigeminal nociceptive system could contribute to the molecular mechanisms that underlie chronic inflammatory TMJ pain.

Transcriptome Analysis of Dorsal Root Ganglion in Rats with Knee Joint Inflammation.

BACKGROUND: Rheumatoid arthritis (RA) leads to pain through alteration of gene expression. Although gene expression alteration in knee cartilage or peripheral blood from RA patients has been identified using microarray, it remains unclear whether long non-coding RNA (lncRNA)-mediated gene regulation occurs in primary sensory neurons of dorsal root ganglia (DRG) during RA-like joint inflammation. In the present study, we aimed to analyze lncRNA and related mRNA profiles in the DRG in a knee joint inflammation rat model. METHODS: Complete Freund's adjuvant (CFA) was injected in the rat knee joint for preparing the joint inflammation model. A lncRNA-mRNA microarray of rat DRG was employed for transcriptome analysis. Functional roles of differentially expressed lncRNAs and their related mRNAs in the injured DRG were delineated by bioinformatic analysis. RESULTS: We observed that expression levels of 9000 lncRNAs were altered on day 7 post-CFA, of which 45.17% were up-regulated and 54.83% were down-regulated. Specifically, 69 lncRNAs (42 up and 27 down) were significantly regulated. We also observed that expression levels of 13,744 mRNAs were altered on day 7 post-CFA, of which 49.67% were up-regulated and 50.33% were down-regulated. Specifically, 102 mRNAs (51 up and 51 down) were significantly regulated. Using quantitative real-time PCR, we verified the changes in differentially expressed lncRNAs in the injured DRG. CONCLUSION: These results suggest that microarray-based RNA sequencing can be used to identify altered lncRNAs and relevant mRNAs in the DRG of rats with knee joint inflammation.

Effects of propofol on invasion and migration of colon cancer cells and JAK2/STAT3 signaling pathway. / ä¸™æ³Šé šå¯¹ç»“è‚ ç™Œç»†èƒžä¾µè¢­è¿ç§»åŠJanusæ¿€é ¶2/信号转导与转录激活子3信号通路的影响.

OBJECTIVES: To investigate the effect of propofol on invasion and migration of human colon cancer cell line SW480 and the JAK2/STAT3 pathway. METHODS: Human colon cancer cell line SW480 was divided into a control group, 3 propofol treatment groups (with 2, 4 and 8 µg/mL propofol treatment, respectively), and a propofol+colivelin group. Lactate dehydrogenase (LDH) activity and cell proliferation was evaluated by detection kit and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) method, respectively. Cell migration and invasion were detected by Transwell assay. Western blotting was performed to detect the protein expression levels of JAK2, p-JAK 2, STAT3 and p-STAT3 in colon cancer cell line SW480. RESULTS: Compared with the control group, the LDH activity was significantly increased in the propofol treatment groups (P<0.05). The cell proliferation, migration, invasion as well as p-JAK2 and p-STAT3 in colon cancer cell line SW480 in the propofol treatment groups were significantly decreased (allP<0.05). Compared with the propofol treatment groups, the p-STAT3 level, proliferation, migration and invasion in the colon cancer cell line SW480 were significantly increased in the propofol+colivelin group (allP<0.05). CONCLUSIONS: Propofol can inhibit the proliferation, migration and invasion of human colon cancer cells by inhibiting JAK2/STAT3 signaling pathway.

Protein kinase C-α upregulates sodium channel Nav1.9 in nociceptive dorsal root ganglion neurons in an inflammatory arthritis pain model of rat.

Previous studies have found that increased expression of Nav1.9 and protein kinase C (PKC) contributes to pain hypersensitivity in a couple of inflammatory pain models. Here we want to observe if PKC can regulate the expression of Nav1.9 in dorsal root ganglion (DRG) in rheumatoid arthritis (RA) pain model. A chronic knee joint inflammation model was produced by intra-articular injection of the complete Freund's adjuvant (CFA) in rats. Nociceptive behaviors including mechanical, cold, and heat hyperalgesia were examined. The expression of Nav1.9 and PKCα in DRG was detected by a quantitative polymerase chain reaction, Western blot, and immunofluorescence. The in vitro and in vivo effects of a PKC activator (phorbol 12-myristate 13-acetate [PMA]) and a PKC inhibitor (GF-109203X) on the expression of Nav1.9 were examined. Moreover, the effects of PKC modulators on nociceptive behaviors were studied. Increased mechanical, heat, and cold sensitivity was observed 3 to 14 days after CFA injection. Parallel increases in messenger RNA and protein expression of Nav1.9 and PKCα were found. Immunofluorescence experiments found that Nav1.9 was preferentially colocalized with IB4+DRG neurons in RA rats. In cultured DRG neurons, PMA increased Nav1.9 expression while GF-109203X prevented the effect of PMA. PMA increased Nav1.9 expression in naïve rats while GF-109203X decreased Nav1.9 expression in RA rats. In naïve rats, PMA caused mechanical and cold hyperalgesia. On the other hand, GF-109203X attenuated mechanical and cold hyperalgesia in RA-pain model. Nav1.9 might be upregulated by PKCα in DRG, which contributes to pain hypersensitivity in CFA-induced chronic knee joint inflammation model of RA pain.

TNFα in the Trigeminal Nociceptive System Is Critical for Temporomandibular Joint Pain.

Previous studies have shown that tumor necrosis factor alpha (TNFα) is significantly increased in complete Freund's adjuvant (CFA)-treated temporomandibular joint (TMJ) tissues. However, it is unclear whether TNFα in the trigeminal nociceptive system contributes to the development of TMJ pain. In the present study, we investigated the role of TNFα in trigeminal ganglia (TG) and spinal trigeminal nucleus caudalis (Sp5C) in CFA-induced inflammatory TMJ pain. Intra-TMJ injection of CFA (10 µl, 5 mg/ml) induced inflammatory pain in the trigeminal nerve V2- and V3-innervated skin areas of WT mice, which was present on day 1 after CFA and persisted for at least 10 days. TNFα in both TG and Sp5C of WT mice was upregulated after CFA injection. The CFA-induced TMJ pain was significantly inhibited in TNFα KO mice. The immunofluorescence staining showed that intra-TMJ CFA injection not only enhanced co-localization of TNFα with Iba1 (a marker for microglia) in both TG and Sp5C but also markedly increased the expression of TNFα in the Sp5C neurons. By the methylated DNA immunoprecipitation assay, we also found that DNA methylation at the TNF gene promoter region in the TG was dramatically diminished after CFA injection, indicating that epigenetic regulation may be involved in the CFA-enhanced TNFα expression in our model. Our results suggest that TNFα in the trigeminal nociceptive system plays a critical role in CFA-induced inflammatory TMJ pain.

[Effect of chitosan porous scaffolds combined with bone marrow mesenchymal stem cells in repair of neurological deficit after traumatic brain injury in rats].

Objective: To investigate the possibility and effect of chitosan porous scaffolds combined with bone marrow mesenchymal stem cells (BMSCs) in repair of neurological deficit after traumatic brain injury (TBI) in rats. Methods: BMSCs were isolated, cultured, and passaged by the method of bone marrow adherent culture. The 3rd generation BMSCs were identified by the CD29 and CD45 surface antigens and marked by 5-bromo-2-deoxyuridine (BrdU). The chitosan porous scaffolds were produced by the method of freeze-drying. The BrdU-labelled BMSCs were co-cultured in vitro with chitosan porous scaffolds, and were observed by scanning electron microscopy. MTT assay was used to observe the cell growth within the scaffold. Fifty adult Sprague Dawley rats were randomly divided into 5 groups with 10 rats in each group. The rat TBI model was made in groups A, B, C, and D according to the principle of Feeney's free fall combat injury. Orthotopic transplantation was carried out at 72 hours after TBI. Group A was the BMSCs and chitosan porous scaffolds transplantation group; group B was the BMSCs transplantation group; group C was the chitosan porous scaffolds transplantation group; group D was the complete medium transplantation group; and group E was only treated with scalp incision and skull window as sham-operation group. Before TBI and at 1, 7, 14, and 35 days after TBI, the modified neurological severity scores (mNSS) was used to measure the rats' neurological function. The Morris water maze tests were used after TBI, including the positioning voyage test (the incubation period was detected at 31-35 days after TBI, once a day) and the space exploration test (the number of crossing detection platform was detected at 35 days after TBI). At 36 days after TBI, HE staining and immunohistochemistry double staining [BrdU and neurofilament triplet H (NF-H) immunohistochemistry double staining, and BrdU and glial fibrillary acidic protein (GFAP) immunohistochemistry double staining] were carried out to observe the transplanted BMSCs' migration and differentiation in the damaged brain areas. Results: Flow cytometry test showed that the positive rate of CD29 of the 3rd generation BMSCs was 98.49%, and the positive rate of CD45 was only 0.85%. After co-cultured with chitosan porous scaffolds in vitrofor 48 hours, BMSCs were spindle-shaped and secreted extracellular matrix to adhere in the scaffolds. MTT assay testing showed that chitosan porous scaffolds had no adverse effects on the BMSCs' proliferation. At 35 days after TBI, the mNSS scores and the incubation period of positioning voyage test in group A were lower than those in groups B, C, and D, and the number of crossing detection platform of space exploration test in group A was higher than those in groups B, C, and D, all showing significant differences ( P<0.05); but no significant difference was found between groups A and E in above indexes ( P>0.05). HE staining showed that the chitosan porous scaffolds had partially degraded, and they integrated with brain tissue well in group A; the degree of repair in groups B, C, and D were worse than that of group A. Immunohistochemical double staining showed that the transplanted BMSCs could survive and differentiate into neurons and glial cells, some differentiated neural cells had relocated at the normal brain tissue; the degree of repair in groups B, C, and D were worse than that of group A. Conclusion: The transplantation of chitosan porous scaffolds combined with BMSCs can improve the neurological deficit of rats following TBI obviously, and also inhabit the glial scar's formation in the brain damage zone, and can make BMSCs survive, proliferate, and differentiate into nerve cells in the brain damage zone.

The interplay of BDNF-TrkB with NMDA receptor in propofol-induced cognition dysfunction : Mechanism for the effects of propofol on cognitive function.

BACKGROUND: The aim of the present study was to verify whether propofol impaired learning and memory through the interplay of N-methyl-D-aspartate (NMDA) receptor with brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (TrkB) signaling pathway. METHODS: 120 Sprague-Dawley (SD) rats were randomly assigned into eight groups. Experimental drugs including saline, intralipid, propofol, N-methyl-D-aspartate (NMDA), 7,8-dihydroxyflavone (7,8-DHF), K252a and MK-801. Spatial learning and memory of rats were tested by the Morris water maze (MWM) test. The mRNA and protein expression were determined by immunohistochemistry, RT-PCR and western blot. Finally, hippocampus cells proliferation and apoptosis were examined by PCNA immunohistochemistry and TUNEL respectively. RESULTS: The memory and learning was diminished in the propofol exposure group, however, the impaired memory and learning of rats were improved with the addition of NMDA and 7,8-DHF, while the improvement of memory and learning of rats were reversed with the addition of K252a and MK-801. In addition, the mRNA and protein expression levels and hippocampus cells proliferation were the same trend with the results of the MWM test, while apoptosis in hippocampus was reversed. CONCLUSION: The propofol can impair memory and learning of rats and induce cognition dysfunction through the interplay of NMDA receptor and BDNF-TrkB-CREB signaling pathway.

MicroRNA-21-5p induces the metastatic phenotype of human cervical carcinoma cells in vitro by targeting the von Hippel-Lindau tumor suppressor.

Numerous studies have indicated that microRNAs (miRs), a group of small non-coding RNAs, are determining regulatory elements involved in the pathogenesis of various types of cancer, including cervical cancer (CC). Although miR-21-5p upregulation has been demonstrated to associate with tumorigenesis by controlling the expression of oncogenic and tumor suppressor genes, only a small number of studies have investigated the expression of miR-21-5p and its functional role in CC. The objective of the present study was to investigate the effect of miR-21-5p on the proliferation, apoptosis, migration and invasion of CC cells, and the potential underlying molecular mechanism of these effects. The measurement of miR-21-5p levels using quantitative polymerase chain reaction revealed that miR-21-5p was markedly increased in CC cell lines compared with normal cells. Upon silencing of miR-21-5p, a marked suppression of the proliferation, migration and invasion of CaSki cells was observed, with induction of cell apoptosis. These effects were reversed with miR-21-5p overexpression. A database search followed by a luciferase reporter assay ascertained that the 3'-untranslated region of the von Hippel-Lindau tumor suppressor (VHL) mRNA sequence was a direct target of miR-21-5p. Furthermore, silencing of VHL neutralized the effects of miR-21-5p inhibition. These observations suggested that miR-21-5p is an oncogene that is able to promote the metastatic phenotype of CC cells through downregulation of VHL expression, which may present a path to novel therapeutic stratagems for the CC therapy.

Effects of different methods of anesthesia and analgesia on immune function and serum tumor marker levels in critically ill patients.

This study investigated the effects of different anesthesia and analgesia methods on immune function and serum tumor marker levels of critically ill patients undergoing tumor resection surgery. Seventy-six critically ill patients with indications for tumor resection surgery were selected in The Second Affiliated Hospital of Zhengzhou University from September 2015 to August 2016. The patients were randomly divided into a control and an observation group (38 patients each). The patients in the control group were treated with general anesthesia and postoperative intravenous analgesia, while the patients in the observation group were treated with general anesthesia and epidural anesthesia and postoperative epidural analgesia. Venous blood samples were collected at 30 min before anesthesia (T1), 2 h after the beginning of the surgery (T2), immediately after surgery (T3), 24 h after surgery (T4) and 72 h after surgery (T5). The viable cell percentage of T lymphocyte subsets (CD3+, CD4+, CD8+, CD4+/CD8+) and natural killer (NK) cells were measured by flow cytometry. The levels of carcinoembryonic antigen, sugar chain antigen 199, sugar chain antigen 125, neuron specific enolase and cytokeratin 19 were detected by electrochemiluminescence at 24 h before and after operation. Our results showed the levels of CD3+, CD4+ and CD4+/CD8+ in the control group at T3-T5 were significantly lower than those at T1 (p<0.05). The CD3+ level in observation group at T3 was also significantly lower than the level at T1 (p<0.05), but it increased at T4 and T5 and showed no significant difference compared with the initial level (p>0.05). The levels of CD4+ and CD4+/CD8+ in the observation group were significantly higher than those in the control group at T2-T5 (p<0.05). And, the levels of CD3+ and CD4+ were significantly higher than those in the control group at T4 (p<0.05). The level of CD4+/CD8+ was significantly higher than that in the control group at T5 (p<0.05). No significant differences were found in the levels of CD8+ and NK cells between the 2 groups at any of the time-points (p>0.05). No significant differences were found either in any of the tested tumor markers in either group after 24 h. Even without differences on the tumor marker levels, these results suggest that general anesthesia combined with epidural anesthesia and analgesia produces milder deleterious effects on the immune function of perioperative critically ill patients than general anesthesia combined with intravenous analgesia.

Epigallocatechin-3-gallate promotes angiogenesis via up-regulation of Nfr2 signaling pathway in a mouse model of ischemic stroke.

Epigallocatechin-3-gallate (EGCG) is the major effective component of green tea and has been known as a potential anticancer drug because of its antioxidant and anti-angiogenic properties. EGCG has also been reported to have preventive effects against ischemic stroke via nuclear factor erythroid 2-related factor 2 (Nfr2) signaling pathway, but how EGCG affect angiogenesis after stroke remains unclear. In this study, we investigated whether EGCG treatment in the acute phase of ischemic stroke can promote angiogenesis in a mouse model of transient middle cerebral artery occlusion (MCAO). We assessed neurological function with modified neurologic severity score (mNSS) test, infarct volume by Nessl staining, angiogenesis and oxidative stress by immunofluorescence analysis, intravital lectin perfusion analysis, western blot analysis and enzyme-linked immunosorbent assay (ELISA). In order to explore the role of Nrf2 in the angiogenesis of MCAO+EGCG-treated mice, we used MAPK/ERK inhibitor PD98059 to block the activation of Nrf2. We found MCAO+EGCG-treated mice had better neurologic outcome, less infarct volume, more number of Ki67/CD31-positive vessels, higher vascular density, unregulated VEGF-VEGFR2 signaling pathway, increased Nrf2 expression and decreased oxidative stress than did MCAO+vehicle-treated mice. Blocking Nrf2 with PD98059 significantly reduced the expression of Nrf2, increased oxidative stress and abolished the angiogenic and neuroprotective effects of EGCG on MCAO mice. We conclude that EGCG treatment in the early stage of ischemic stroke can promote angiogenesis in MCAO mice, possibly via upregulation of Nrf2 signaling pathway.

Effect of dexmedetomidine on cerebral ischemia-reperfusion rats by activating mitochondrial ATP-sensitive potassium channel.

The aim of the study reported here was to evaluate whether the mitochondrial ATP-sensitive potassium (mitoKATP) channel could participate in the effect of dexmedetomidine on cerebral ischemia-reperfusion (I/R) rats. Forty rats were randomly assigned into 5 groups: sham operation (S) group; cerebral I/R group; dexmedetomidine (D) group; 5-hydroxydecanoate (5-HD) group; 5-HD + D group. The cerebral I/R were produced by 2 h right middle cerebral artery occlusion followed by 24 h reperfusion. Dexmedetomidine (50µg/kg) was injected intraperitoneally before ischemia and after the onset of reperfusion. 5-HD (30 mg/kg) was injected intraperitoneally at 1 h before ischemia. The neurological deficit score (NDS) and the levels of super oxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO), Interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were evaluated. Compared to group S, NDS and the levels of MDA, MPO, IL-6 and TNF-α were significantly higher, and SOD levels were significantly lower in the other groups (P < 0.05). Compared to group I/R,NDS and the levels of MDA, MPO, IL-6 and TNF-α were significantly lower, and SOD level was significantly higher in group D (P < 0.05). Compared to group D, NDS and the levels of MDA, MPO, IL-6 and TNF-α were significantly higher, and SOD level was significantly lower in group5-HD + D (P < 0.05). The activation of the mitoKATP channel could contribute to the protective effect of dexmedetomidine on rats induced by focal cerebral ischemia-reperfusion injury.

Dexmedetomidine-fentanyl versus propofol-fentanyl in flexible bronchoscopy: A randomized study.

The aim of the present study was to evaluate the effect of a combination of dexmedetomidine and fentanyl on peripheral oxygen saturation (SpO2) and hemodynamic stability in patients undergoing flexible bronchoscopy. One hundred patients undergoing elective flexible bronchoscopy were randomized into either a propofol-fentanyl group (PF group; n=50) or a dexmedetomidine-fentanyl group (DF group; n=50). SpO2 values, heart rate (HR), systolic and diastolic blood pressure (SBP and DBP), patients' cough scores and discomfort scores as determined by patients and bronchoscopists, levels of sedation, number of times that additional lidocaine was required, elapsed time until recovery, and adverse events were recorded. The mean SpO2 values in the DF group were significantly higher than those in the PF group (P<0.01), and HR, SBP and DBP were significantly lower in the DF group than in the PF group (P<0.05). There were no statistically significant differences between the two groups in terms of cough scores or discomfort scores, sedation levels, or number of times that additional lidocaine was required (P>0.05). Elapsed time until recovery in the DF group was significantly longer than in the PF group (P=0.002). The incidence of hypoxemia was significantly lower in the DF group than in the PF group (P=0.027), but the incidence of bradycardia was significantly higher in the DF group than in the PF group (P=0.037). Dexmedetomidine-fentanyl was superior to propofol-fentanyl in providing satisfactory SpO2. Furthermore, dexmedetomidine-fentanyl attenuated hemodynamic responses during bronchoscopy and maintained hemodynamic stability in the early stage of the procedure.

Inhibition of MicroRNA-221 Alleviates Neuropathic Pain Through Targeting Suppressor of Cytokine Signaling 1.

Neuropathic pain results in considerable trouble to people's physical and mental health. The pathophysiological mechanisms underlying its occurrence and development remain unclear. A large number of experiments show that microRNAs (miRNAs) play a major role in the pathogenesis of neuropathic pain and neuroinflammation resulting from nerve injury. Among various miRNAs, microRNA-221 (miR-221) overexpression has been reported in a chronic constrictive injury (CCI)-induced rat model of neuropathic pain. However, the role of miR-221 in the regulation of neuropathic pain is unknown. In this study, we investigated the potential role and underlying mechanism of miR-221 in regulating neuropathic pain. Our findings show that miR-221 is overexpressed in the spinal cord and the isolated microglia of CCI rats. Intrathecal injection of a miR-221 inhibitor attenuated CCI-induced mechanical allodynia and thermal hyperalgesia, and reduced proinflammatory cytokine expression, including tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 in CCI rats. Using a dual-luciferase reporter assay, we show that suppressor of cytokine signaling 1 (SOCS1), an important regulator of inflammation, is a direct target of miR-221. Treatment with the miR-221 inhibitor significantly inhibited the expression of SOCS1. Furthermore, the miR-221 inhibitor markedly suppressed the activation of nuclear factor-kappa B (NF-κB) and the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway. Knockdown of SOCS1 in CCI rats abrogated the inhibitory effect of the miR-221 inhibitor on CCI-induced neuropathic pain and the NF-κB and p38 MAPK signaling pathways. Together, these results suggest that inhibition of miR-221 alleviates neuropathic pain and neuroinflammation through increasing SOCS1 and by inhibiting the NF-κB and p38 MAPK signaling pathways, indicating that miR-221 may be a promising molecular target for the treatment of neuropathic pain.

Impact of CYP2D6 Polymorphisms on Postoperative Fentanyl Analgesia in Gastric Cancer Patients.

BACKGROUND: This study investigated the influence of human cytochrome P450 2D6 (CYP2D6) gene polymorphism in gastric cancer (GC) patients to understand the pharmacogenomic basis for patient response to postoperative fentanyl analgesia. METHODS: The prospective study design contained 212 patients recovering from radical gastrectomy. Peripheral blood samples were collected after general anesthesia, and CYP2D6 genotypes were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. After providing adequate instructions to operate the analgesia pump, patients self-administered fentanyl via patient controlled intravenous analgesia. The cumulative amount of fentanyl self-administered and the associated adverse effects were recorded at 6, 12, 24, and 48 h postoperatively. RESULTS: Five patients, out of the 212 patients recruited to this study, failed to complete the study. The remaining 207 patients were classified into three groups based on their genotypes: W/W group (n=44), M/W group (n=112), and M/M group (n=51). Our results demonstrated that the cumulative amount of fentanyl consumption significantly increased in the M/M group at 6, 12, and 24 h postoperatively, compared with the W/W group (p<0.05). In addition, visual analogue scale (VAS) score in the M/M group was significantly higher than the W/W group in the analepsia period after general anesthesia and at 6 h postoperatively (p<0.05). No significant adverse effects were observed in all the groups (p>0.05). CONCLUSION: CYP2D6 polymorphism influenced patient response to postoperative fentanyl analgesia in GC patients.

Intravenous dezocine pretreatment reduces the incidence and intensity of myoclonus induced by etomidate.

To evaluate the suppressive effect of intravenous dezocine on the incidence and severity of myoclonic movements induced by etomidate, a total of 80 patients, American Society of Anesthesiologists physical status I-II, were randomized into two equally sized groups (n = 40). These two groups were assigned to give either intravenous dezocine 0.1 mg/kg or a matching placebo (equal volume of 0.9% saline) 30 s before administration of etomidate. For anesthesia induction, 0.3 mg/kg etomidate was injected over a period of 1 min. One minute after etomidate administration, the severity of myoclonus was assessed. Pretreatment with dezocine significantly reduced both the incidence and intensity of myoclonus. These results demonstrate that intravenous dezocine 0.1 mg/kg 30 s prior to induction was effective in suppressing myoclonic movements in our patients.