Dehydro ketomethylene and ketomethylene analogs of substance P: synthesis and biological activity

1988 ◽  
Vol 31 (2) ◽  
pp. 416-421 ◽  
Author(s):  
Ariel Ewenson ◽  
Ralph Laufen ◽  
Michael Chorev ◽  
Zvi Selinger ◽  
Chaim Gilon
1999 ◽  
Vol 276 (4) ◽  
pp. G875-G885 ◽  
Author(s):  
N. A. Deshpande ◽  
T. J. McDonald ◽  
M. A. Cook

Isolated myenteric ganglion networks were used in a perifusion protocol to characterize the response of interstitial adenosine levels to changes in prevailing[Formula: see text]. The biological activity of such adenosine was assessed using inhibition of release of substance P (SP) as a functional measure of adenosine activity, and the effect of altered O2 tension on both spontaneous and elevated extracellular K+ concentration-evoked SP release from networks was determined over a range of[Formula: see text] values from hypoxic ([Formula: see text] = 54 mmHg) to hyperoxic ([Formula: see text] = 566 mmHg). Release of SP was found to be sensitive to [Formula: see text], and a linear graded relationship was obtained. Perifusion in the additional presence of the adenosine A1-receptor-selective antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) revealed considerable adenosinergic inhibition with an inverse exponential relationship and hyperoxic threshold [Formula: see text]. Disinhibition of evoked SP release by DPCPX in the absence of TTX was double that observed in its presence, indicating a neural source for some of the adenosine released during hypoxia. A postulated neuroprotective role for adenosine is consistent with the demonstrated relationship between interstitial adenosine and prevailing O2 tension.


1982 ◽  
Vol 25 (10) ◽  
pp. 1209-1213 ◽  
Author(s):  
Mark C. Allen ◽  
Derek E. Brundish ◽  
Roy Wade ◽  
Bengt E. B. Sandberg ◽  
Michael R. Hanley ◽  
...  

1993 ◽  
Vol 193 (2) ◽  
pp. 624-630 ◽  
Author(s):  
Y. Shimohigashi ◽  
H. Matsumoto ◽  
Y. Takano ◽  
R. Saito ◽  
T. Iwata ◽  
...  

Biopolymers ◽  
1993 ◽  
Vol 33 (6) ◽  
pp. 915-926 ◽  
Author(s):  
M. Tallon ◽  
D. Ron ◽  
D. Halle ◽  
P. Amodeo ◽  
G. Saviano ◽  
...  

2009 ◽  
Vol 37 (3) ◽  
pp. 180-184 ◽  
Author(s):  
GEORGE STAVROPOULOS ◽  
KOSTAS KARAGIANNIS ◽  
PAUL CORDOPATIS ◽  
DAVID HALLE ◽  
CHAIM GILON ◽  
...  

Pain Medicine ◽  
2020 ◽  
Vol 21 (12) ◽  
pp. 3443-3450
Author(s):  
Chao Yang ◽  
Yunheng Sun ◽  
Xueyan Ouyang ◽  
Jing Li ◽  
Zhen Zhu ◽  
...  

Abstract Background In a previous study, persistent pain was suggested to be a risk factor for tumor patients. However, the mechanism underlying this phenomenon is still unclear. Substance P (SP), a pain-related neuropeptide secreted by the neural system and the immune system, plays an important role in the induction and maintenance of persistent pain. Methods In this study, in order to explore whether SP participates in the influence of pain on tumor progression, the serum samples of lung cancer and breast cancer patients were collected and tested. An elevated expression of SP was found in patients with pain. Results Cell pharmacological experiments revealed that SP can upregulate the expression of Toll-like receptor-4 (TLR-4) in tumor cells and increase the proliferation, migration, and invasive activity of tumor cells. As high expression of TLR-4 has the ability to enhance the biological activity of tumor cells, TLR-4 is thought to be involved in SP-induced tumor proliferation, migration, and invasion. Treatment of tumor cells with Aprepitant, a specific blocker of the NK-1 receptor, could reduce the expression of TLR-4 and reduce the proliferation, invasion, and migration activities of tumor cells; further proof of the influence of SP on TLR-4 expression depends on the NK-1 receptor located in tumor cells. Conclusions Based on the results above, we proposed a possible mechanism underlying pain affecting tumor progression: The presence of pain increases the content of SP in patients’ blood, and elevated SP increases the expression of tumor TLR-4 by acting on the NK-1 receptor, which ultimately affects the biological activity of the tumor.


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