Key Laboratory for Gastrointestinal Diseases of Gansu Province

Lanzhou, China

Key Laboratory for Gastrointestinal Diseases of Gansu Province

Lanzhou, China

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He C.,Institute of Biochemistry and Molecular Biology | Gong J.,Institute of Biochemistry and Molecular Biology | Yang L.,Institute of Biochemistry and Molecular Biology | Zhang H.,Institute of Biochemistry and Molecular Biology | And 4 more authors.
Canadian Journal of Physiology and Pharmacology | Year: 2016

The present study focused on the interactive pain regulation of endokinin A/B (EKA/B, the common C-terminal decapeptide in EKA and EKB) or endokinin C/D (EKC/D, the common C-terminal duodecapeptide in EKC and EKD) on chimeric peptide MCRT (YPFPFRTic-NH2, based on YPFP-NH2 and PFRTic-NH2) at the supraspinal level in mice. Results demonstrated that the co-injection of nanomolar EKA/B and MCRT showed moderate regulation, whereas 30 pmol EKA/B had no effect on MCRT. The combination of EKC/D and MCRT produced enhanced antinociception, which was nearly equal to the sum of the mathematical values of single EKC/D and MCRT. Mechanism studies revealed that pre-injected naloxone attenuated the combination significantly compared with the equivalent analgesic effects of EKC/D alone, suggesting that EKC/D and MCRT might act on two totally independent pathways. Moreover, based on the above results and previous reports, we made two reasonable hypotheses to explain the cocktail-induced analgesia, which may potentially pave the way to explore the respective regulatory mechanisms of EKA/B, EKC/D, and MCRT and to better understand the complicated pain regulation of NK1 and µ opioid receptors, as follows: (1) MCRT and endomorphin-1 possibly activated different µ subtypes; and (2) picomolar EKA/B might motivate the endogenous NPFF system after NK1 activation. © 2016, Canadian Science Publishing. All rights reserved.


Zhou L.,Lanzhou University | Zhou L.,Key Laboratory for Gastrointestinal Diseases of Gansu Province | Yang Q.,Institute of Biochemistry and Molecular Biology | He C.,Institute of Biochemistry and Molecular Biology | And 4 more authors.
Neuropeptides | Year: 2015

The present study focused on the interactive effects of (Mpa6)-γ2-MSH-6-12 (Mpa, spinal level) and endokinin A/B (EKA/B, supraspinal level) on pain regulation in mice. EKA/B (30pmol) only weakened 100pmol Mpa-induced hyperalgesia at 5min, but could enhance it during 20-30min. However, EKA/B (100pmol) antagonized all dose levels of Mpa significantly at 5min and blocked them completely at 10min. EKA/B (3nmol) co-injected with Mpa presented marked analgesia at 5min and enduring hyperalgesia within 20-60min. To investigate the underlying mechanisms between Mpa and EKA/B, SR140333B and SR142801 (NK1 and NK3 receptor antagonists, respectively) were utilized. SR140333B had no influence on Mpa, while SR142801 potentiated it during 20-30min. Whereas, SR140333B and SR142801 could block the co-administration of Mpa and EKA/B (30pmol) separately at 5min and 30min. These phenomena might attribute to that these two antagonists promoted the antagonism of EKA/B (30pmol) at the early stage, while antagonized EKA/B preferentially in the latter period. SR140333B weakened the analgesia of EKA/B (3nmol), but produced no effect on Mpa. However, SR140333B failed to affect the co-injection of Mpa and EKA/B, which implied that EKA/B cooperated with Mpa prior to SR140333B. These results could potentially help to better understand the interaction of NK and MrgC receptors in pain regulation in mice. © 2015 Elsevier Ltd.


Chen Z.-F.,Lanzhou University | Chen Z.-F.,Key Laboratory for Gastrointestinal Diseases of Gansu Province | Huang S.-S.,Lanzhou University | Liu M.,Lanzhou University | And 13 more authors.
Journal of Practical Oncology | Year: 2014

Objective: To investigate the mechanisms related to the expression of E-cadherin regulated by COX-2 in human gastric cancer cells. Methods: Human gastric cancer SGC-7901 cells were treated with cyclooxygenase-2 (COX-2) inhibitor, celecoxib, at different concentrations for different durations. Western blot and real time quantitative RT-PCR were used to detect mRNA and protein expression of COX-2, NF-κB, Snail and E-cadherin. Results: The mRNA and protein expressions of COX-2, NF-κB and Snail in SGC-7901 cells declined and those of E-cadherin increased significantly after treated with celecoxib (P<0.05), in a dose- and time-dependent manner. The expression of COX-2 was positively correlated with NF-κB (r=0.881, P<0.01) and Snail (r=0.839, P<0.01) level, and was negatively correlated with E-cadherin level (r=-0.814, P<0.01). Conclusion: COX-2 may regulate the expression of E-cadherin through NF-κB and Snail signaling pathway during gastric cancer progression.

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