The First Hospital of Shijiazhuang
The First Hospital of Shijiazhuang
Wen D.,Hebei Medical University |
Ma C.-L.,Hebei Medical University |
Zhang Y.-J.,The First Hospital of Shijiazhuang |
Meng Y.-X.,Hebei Medical University |
And 3 more authors.
BMC Neuroscience | Year: 2012
Background: Cholecystokinin octapeptide (CCK-8), the most potent endogenous anti-opioid peptide, has been shown to regulate the processes of morphine dependence. In our previous study, we found that exogenous CCK-8 attenuated naloxone induced withdrawal symptoms. To investigate the precise effect of exogenous CCK-8 and the role of cholecystokinin (CCK) 1 and/or 2 receptors in morphine dependence, a SH-SY5Y cell model was employed, in which the μ-opioid receptor, CCK1/2 receptors, and endogenous CCK are co-expressed.Results: Forty-eight hours after treating SH-SY5Y cells with morphine (10 μM), naloxone (10 μM) induced a cAMP overshoot, indicating that cellular morphine dependence had been induced. The CCK receptor and endogenous CCK were up-regulated after chronic morphine exposure. The CCK2 receptor antagonist (LY-288,513) at 1-10 μM inhibited the naloxone-precipitated cAMP overshoot, but the CCK1 receptor antagonist (L-364,718) did not. Interestingly, CCK-8 (0.1-1 μM), a strong CCK receptor agonist, dose-dependently inhibited the naloxone-precipitated cAMP overshoot in SH-SY5Y cells when co-pretreated with morphine. The L-364,718 significantly blocked the inhibitory effect of exogenous CCK-8 on the cAMP overshoot at 1-10 μM, while the LY-288,513 did not. Therefore, the CCK2 receptor appears to be necessary for low concentrations of endogenous CCK to potentiate morphine dependence in SH-SY5Y cells. An additional inhibitory effect of CCK-8 at higher concentrations appears to involve the CCK1 receptor.Conclusions: This study reveals the difference between exogenous CCK-8 and endogenous CCK effects on the development of morphine dependence, and provides the first evidence for the participation of the CCK1 receptor in the inhibitory effects of exogenous CCK-8 on morphine dependence. © 2012 Wen et al.; licensee BioMed Central Ltd.
Zhang B.,Hebei Medical University |
Zhang J.-W.,Hebei Medical University |
Wang W.-P.,Hebei Medical University |
Dong R.-F.,Cangzhou central Hospital |
And 2 more authors.
Synapse | Year: 2017
Purpose: Lamotrigine (LTG) is a broad-spectrum antiepileptic drug that is widely used in clinic. However, the effect of LTG on cognition and neurodegeneration during epilepsy treatment remains controversial. In this study, we compared the cognitive effects of LTG and sodium valproate in pentylenetetrazole (PTZ)-kindled animal model, and the dose dependency was tested for LTG. Methods: PTZ-kindled animals were divided into the following treatment groups: control group, treated with 3.5 mL/kg of 0.9% sodium chloride; low-dose LTG group, treated with 12.5 mg/kg of LTG; middle-dose LTG group, treated with 25 mg/kg of LTG; high-dose LTG group, treated with 50 mg/kg of LTG; VPA group, treated with 300 mg/kg of VPA. The Morris Water Maze (MWM) test commenced from the 10th day of treatment. Hippocampal cell apoptosis was determined by TUNEL staining after two weeks of treatment. Results: Compared to the vehicle-treated control group, escape latency was significantly reduced in the middle- and high-dose LTG- and VPA-treated groups on the 3rd and 4th day of the MWM test (p <.05), and spatial probe frequency was significantly improved in the middle- and high-dose LTG- and VPA-treated groups (p <.05). Furthermore, the immunohistochemical score of TUNEL positive cells significantly decreased in the hippocampal CA1 region in the middle- and high-dose LTG- and VPA-treated groups (p <.05). Conclusion: Our data suggests that LTG may ameliorate epilepsy-induced cognitive impairment and neuronal cell apoptosis during epilepsy treatment. LTG may ameliorate cognitive impairment and neuronal cell apoptosis during epilepsy treatment. © 2016 The Authors Synapse Published by Wiley Periodicals, Inc.
Fan Y.,The First Hospital of Shijiazhuang |
Zhang S.,The First Hospital of Shijiazhuang |
Liang F.,The First Hospital of Shijiazhuang |
Zhou Y.,The First Hospital of Shijiazhuang |
Zhang C.,The First Hospital of Shijiazhuang
International Journal of Clinical and Experimental Pathology | Year: 2017
Osteoporosis is a systemic metabolic and serious skeletal disease commonly observed among the elderly. Insulin-like growth factors (IGFs) are critical regulators for bone cell function. We estimated the role of IGF-I rs35767, rs2288377 and rs5742612 polymorphisms in the susceptibility to osteoporosis in a population of China, and assessed gene-environment interactions. A total of 346 patients with osteoporosis and 346 controls were enrolled. Genotyping of IGF-I rs35767, rs2288377 and rs5742612 was amplified and performed with the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The TA and AA genotypes displayed elevated risk of developing osteoporosis (TA vs TT: OR=1.54, 95% CI=1.11-2.15; AA vs TT: OR=3.65, 95% CI=2.09-6.37). Compared with TT individuals, individuals with the TA+AA genotype had a substantial increased susceptibility to osteoporosis (OR=1.80, 95% CI=1.31-2.46). In recessive model, the AA genotype of rs2288377 displayed 2.89 folds risk of osteoporosis (adjusted OR=2.89, 95% CI=1.70-4.89). A significant negative interaction was found between IGF-I rs2288377 and BMD levels for femoral neck (r=-0.14, P < 0.001), total hip (r=-0.09, P < 0.001) and trochanter (r=-0.13, P < 0.001). In conclusion, we suggest that IGF-I rs2288377 polymorphism had a strong influence on osteoporosis susceptibility in this Chinese population.
Shang Y.,Hebei University |
Zang A.,Hebei University |
Li J.,Hebei University |
Jia Y.,Hebei University |
And 9 more authors.
Biomedicine and Pharmacotherapy | Year: 2016
Purpose The purpose of this study is to examine the expression and clinical significance microRNA-383 (miR-383) in non-small cell lung cancer (NSCLC) both in vitro and in vivo. Methods Tumorous miR-383 expressions were compared between NSCLC cell lines and normal lung cells. MiR-383 was upregulated in A549 and H596 cells to evaluate its tumor suppressive effect on NSCLC proliferation, invasion and migration in vitro. MiR-383 expression was also compared between 139-paired clinical NSCLC tissues and their adjacent non-carcinoma lung tissues, as well as between early-stage NSCLC tissues and advanced-stage NSCLC tissues. Correlation between tumorous miR-383 expression and NSCLC patients’ clinicopathological features and overall survival (OS) were also statistically analyzed. Results MiR-383 was significantly downregulated in NSCLC cell lines. MiR-383 overexpression reduced proliferation, invasion and migration of A549 and H596 cells. In clinical samples, miR-383 was also found to be markedly downregulated in NSCLC carcinomas than in non-carcinoma lung tissues, and in advanced-stage carcinomas than in early-stage carcinomas. It was also found low tumorous miR-383 expression was significantly associated with NSCLC patients’ poor prognosis, including advanced TNM stages, positive lymph node metastasis, and shorter OS. Conclusion Endogenous miR-383 is a functional tumor suppressor in NSCLC. It may also serve as an independent prognostic factor for patients with NSCLC. © 2016 Elsevier Masson SAS
Liu L.,Hebei Medical University |
Liu N.,The First Hospital of Shijiazhuang |
Zhao Z.,Hebei Medical University |
Liu J.,The First Hospital of Shijiazhuang |
And 3 more authors.
Liver International | Year: 2012
Background/Aim: TNF-α is increased in hepatopulmonary syndrome (HPS). Pentoxifylline (PTX) mitigated experimental HPS through the inhibition of TNF-α. However, PTX has pleiotropic effects besides the inhibition of TNF-α. This study is to neutralize TNF-α with specific monoclonal antibody to TNF-α (TNF-α McAb) to investigate the effect of TNF-α on HPS. Materials and methods: Hepatopulmonary syndrome was induced by common bile duct ligation (CBDL); controls were sham operated. The endpoints were 1, 2, 3, 4 and 5 weeks after surgery. 99mTechnetium-macroaggregated albumin (Tc-MAA) was to evaluate intrapulmonary arteriovenous shunts; Portal venous pressure, cardiac output and mean blood pressure (MAP) were also measured. Serum was for Alanine transaminase (ALT), endotoxin, TNF-α and nitric oxide (NO) measurements, liver for histology, lung for histology and iNOS, PI3K/Akt expression assay. Results: Portal vein pressure was significantly elevated and MAP decreased in CBDL rats. Tc-MAA was mainly located in lung and very weak in brain in sham group and mainly in brain of CBDL rats. TNF-α McAb significantly decreased the radioactivity in the brain, reduced cardiac output, increased MAP and systemic vascular resistance (SVR) in CBDL animals. Serum ALT, endotoxin, TNF-α and NO were significantly increased. TNF-α McAb significantly decreased these serum indices in CBDL rats. TNF-α McAb significantly alleviated liver damage, decreased alveolar-arterial gradient and inhibited iNOS, PI3K/Akt and p-Akt expression in lung tissue. Furthermore, TNF-α McAb significantly attenuated the inflammatory response in lung. Conclusion: TNF-α McAb improves HPS in cirrhotic rats; this effect is likely mediated through the inhibition of TNF-α PI3K/Akt-NO pathway. © 2012 John Wiley & Sons A/S.
Zhang Y.,The First Hospital of Shijiazhuang |
Li L.,The First Hospital of Shijiazhuang |
Xiang C.,The First Hospital of Shijiazhuang |
Ma Z.,The First Hospital of Shijiazhuang |
And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2013
The aim of this in vivo study was to explore the protective properties of melatonin against Adriamycin-induced myocardial toxicity. A rat model of breast cancer was established and the rats were randomly divided into the blank group (Blank), the solvent group [Diss; dehydrated alcohol: physiological saline (1:9)], the Adriamycin group (ADM), the melatonin group (MLT) and the melatonin + Adriamycin group (M+A). The concentrations of lipid peroxide (LPO), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in myocardial tissues were detected, the changes in myocardial tissues were observed using light microscopy and electron microscopy, and the 1-month survival rates of each group of rats were compared. Breast cancer was established in 116 rats. In the ADM group, the concentration of LPO was higher and the concentrations of SOD and GSH-Px were significantly lower than those in the blank group. In the M+A group, compared with the ADM group, the concentration of LPO was lower (P<0.05) and the concentrations of SOD and GSH-Px were higher (P<0.05). It was observed using light and electron microscopy that the myocardial injuries to the M+A group were significantly alleviated in comparison with those in the ADM group; the 1-month survival rate in the M+A group was higher than that in the ADM group. Melatonin may have a protective role in the myocardium by reducing Adriamycin-induced myocardial oxidative damage.
Han X.,Hebei Medical University |
Hou S.,The First Hospital of Shijiazhuang |
Yang A.,Hebei Medical University
Medical Science Monitor | Year: 2016
Background: Diabetes mellitus a common metabolic disorder with hyperglycemia, is caused by the interaction of genetic and environmental factors. Approximately 12~20% of diabetic patients have risk of colorectal cancer. Recent studies revealed that the insulin-like growth factor system (IGFs) plays an important role in tumor occurrence. This study thus investigated the relationship between IGFs-related proteins in diabetic patients and the incidence of colorectal carcinoma. Material/Methods: A retrospective study was performed in a total of 206 individuals, including 85 diagnosed with diabetes. The incidence of colorectal cancer was tracked, along with the detection of IGFs expression in serum. During the surgical resection, tumor tissues and adjacent tissues were collected and quantified for IGFs expression level. Results: We found no significant difference in age or sex between the diabetic and control groups. Diabetic patients, however, had elevated body weight and higher incidence of colorectal cancer compared to non-diabetic controls (p<0.05). The diabetic group also had higher IGF-I and IGF-IR mRNA levels in serum, while IGFBP-6 expression was down-regulated. In comparison to adjacent healthy tissues, tumor tissue had higher levels of IGF-I and IGF-IR but lower levels of IGFBP-6 (p<0.05). Conclusions: Our study showed higher incidence of colorectal cancer in diabetics compared to non-diabetics. The occurrence of colorectal cancer in diabetic patients may be associated with elevated IGFs-related protein expression level. © Med Sci Monit.
PubMed | The First Hospital of Shijiazhuang and Hebei Medical University
Type: Journal Article | Journal: Journal of physiology and biochemistry | Year: 2016
miR-148b has been found to be aberrantly expressed in various tumor types. It has recently been reported to be involved in regulating radioresistance in non-small cell lung cancer (NSCLC) cells. However, its expression level and association with radiosensitivity in human patient samples have not been investigated. Real-time PCR was used to evaluate the expression levels of miR-148b. (2) test was performed to analyze the association between miR-148b expression levels and clinicopathological factors or radiosensitivity. Kaplan-Meier survival curve was constructed to estimate the overall survival (OS), and the differences in survival were compared using the log-rank test. Cox regression analysis was conducted to determine the prognostic value of miR-148b. The relative level of miR-148b was significantly decreased in NSCLC tissues compared with matched non-cancerous tissues (P<0.0001), and it was higher in tissues of patients who are good responders compared to those who are poor responders to radiotherapy (P<0.0001). Lower expression of miR-148b was positively associated with high tumor stage (P=0.0407) and radioresistance (P=0.0002), and it predicted poor survival in patients with (P=0.0129) or without (P=0.0094) radiotherapy treatment. miR-148b was an independent prognostic factor for NSCLC as demonstrated by Cox proportional hazards risk analysis. miR-148b may serve as a prognostic biomarker of poor survival and a novel predictor of response to radiotherapy treatment in NSCLC.
PubMed | First Hospital of Shijiazhuang, Affiliated Hospital to Chengde Medical College and The First Hospital of Shijiazhuang
Type: | Journal: Disease markers | Year: 2016
To investigate the correlation and significance between the urine soluble Fas (sFas) and vascular endothelial growth factor (VEGF) expression in patients with urothelial bladder carcinoma (UC).The level of sFas was measured by enzyme-linked immunosorbent assay (ELISA) and the expression of VEGF protein in UC surgical specimens was screened by immunohistochemical method. These data were analyzed through SPSS 13.0 software.The urinary sFas levels were significantly higher in the patients with UC than in those without cancer (168.0ng/mL 84.6 versus 56.2ng/mL 37.0; P < 0.05) and in the cases with a higher stage or grade than in those with a lower stage or grade (each P < 0.05). They had a positive relationship between the expression of VEGF protein and the pathological stage or grade in UC tissues (each P < 0.05). Spearman rank correlation test showed a significant correlation between sFas levels and VEGF expressions (R = 0.882, P < 0.05).The effects of sFas and VEGF may play important roles together in the occurrence and progression of UC. Joint detection of urine sFas plus VEGF protein may provide valuable solutions to improve the diagnosis and treatment of UC.
PubMed | Hebei General Hospital, The First Hospital of Shijiazhuang, Bethune International Peace Hospital and The Sixth Hospital of Shijiazhuang
Type: Journal Article | Journal: Neurochemical research | Year: 2016
Opioid analgesics have less efficacy in diabetic neuropathy treatment, and tolerance often occurs after chronic usage. Given that thalidomide can potentiate the morphine efficacy in diabetic neuropathy treatment, we investigated the effects of intrathecal administrations of thalidomide on morphine tolerance during the treatment of diabetic neuropathy. We found that intrathecal administrations of thalidomide (25mg/kg/ml) potentiated the analgesic effects of morphine on mechanical hyperalgesia and prevented the development of morphine tolerance. While this treatment regimen did not alter the protein levels of -opioid receptor (MOR) in the spinal cord of diabetic rats, chronic morphine treatment robustly increased MOR binding density in the synaptic plasma membranes fraction, but decreased it in the microsomal fraction. Furthermore, thalidomide was able to reverse the distribution of MOR altered by chronic morphine treatment. Finally, STZ-induced diabetes promoted PKC activation and enhanced TNF level in the spinal cord, which were attenuated by intrathecal administrations of thalidomide. Taken together, these results suggested that thalidomide may potentiate morphine efficacy on diabetic neuropathy and prevent the development of morphine tolerance by suppressing PKC activation and TNF level in the spinal cord.