Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Analysis of somatostatin-like immunoreactivity (SLI) in guinea pig brain by HPLC and radioimmunoassay revealed an unexpected peak of SLI eluting at a retention time slightly later than standard somatostatin-14. The following evidence argues that this peak represents dihydro (H2) somatostatin-14. (1) The peak had the same retention time as standard [H2]somatostatin. (2) The possibility of a reduction artefact due to tissue processing was excluded by adding exogenous somatostatin-14 or 125I-labeled N-Tyr-somatostatin-14 to tissue and observing that no corresponding reduced peptides were generated. (3) Mild oxidation of brain extracts with H2O2 decreased, whereas mild reduction with dithiothreitol increased, the proposed peak of [H2]somatostatin. (4) Reaction of tissue extracts with iodoacetamide decreased the size of the proposed [H2]somatostatin peak but resulted in generation of a new peak co-eluting with standard carboxymethylated somatostatin-14. The proportion of the [H2]somatostatin peak in five brain regions, the hypothalamus, amygdala, cerebral cortex, brainstem and cerebellum, ranged from 6 to 20% of total SLI. The probability of somatostatin-14 existing endogenously in reduced or oxidized forms may have implications for its biological function in the guinea pig.
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PMID:Evidence for the presence of dihydro (reduced) somatostatin-14 in the guinea pig brain. 289 59

We propose an improved silver procedure for intensification of peroxidase staining. It utilizes the high argyrophilia of polymerized Ni-DAB as a chromogen of peroxidase histochemistry, and the capacity of Cu++-catalyzed H2O2 oxidation to suppress tissue argyrophilia without influencing the argyrophilia of the polymerized Ni-DAB. This procedure is much more effective than any previously proposed intensification technique. When used in somatostatin histochemistry, it reveals perikarya, fibers, and nerve terminals in locations at which they have never been detected in preparations where only the DAB polymer was silver-intensified.
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PMID:Copper-H2O2 oxidation strikingly improves silver intensification of the nickel-diaminobenzidine (Ni-DAB) end-product of the peroxidase reaction. 289 97

Recent studies have shown that somatostatin modulates lymphocyte function, but the effects of somatostatin on macrophage function are not clearly defined. In the present study, peritoneal macrophages (Mluminal diameter) obtained from male rats were treated in vitro with somatostatin or octreotide and their effects on the release of hydrogen peroxide (H2O2), nitrite, and tumor necrosis factor (TNF) determined. Macrophages treated with somatostatin (10(-9) M to 10(-7) M) or octreotide (10(-8) M and 10(-7) M) released significantly greater amounts of PMA-stimulated H2O2 than did the untreated controls. In addition, 10(-9) M of somatostatin significantly enhanced PMA-stimulated H2O2 release by LPS-treated Mluminal diameter. Octreotide had no effect on H2O2 release by LPS-treated Mluminal diameter. At concentrations of 10(-14) M, 10(-13) M, or greater than 10(-8) M, somatostatin or octreotide suppressed nitrite release by Mluminal diameter. Somatostatin or octreotide did not affect nitrite release by LPS-treated Mluminal diameter. On the other hand, Mluminal diameter treated with 10(-11) M of somatostatin or octreotide released greater amounts of TNF than did the untreated controls. In contrast, TNF release by Mluminal diameter treated with 10(-9) M to 10(-5) M of somatostatin or 10(-7) M to 10(-5) M of octreotide was less than that of the controls. Anti-TNF antibody (1:1000) caused a reduction in the release of H2O2 and nitrite. These findings demonstrate that somatostatin and octreotide modulate the release of H2O2, nitric oxide, and TNF by Mluminal diameter depending on the concentration of hormones used.
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PMID:Somatostatin and macrophage function: modulation of hydrogen peroxide, nitric oxide and tumor necrosis factor release. 857 Aug 54

Recent studies have shown that somatostatin modulates lymphocyte and peritoneal macrophage function, but the effects of somatostatin on hepatic macrophages (Kupffer cells) are not clearly defined. In the present study, hepatic macrophages obtained from male rats were treated in vitro with somatostatin or octreotide and their effects on the release of nitrite, tumor necrosis factor (TNF), and hydrogen peroxide (H2O2) determined. At concentrations of 10(-14) M to 10(-12) M, or greater than 10(-10) M, somatostatin suppressed nitrite release by Kupffer cells. At concentrations of less than 10(-9) M or greater than 10(-9) M, octreotide inhibited nitrite release by Kupffer cells. Kupffer cells treated with 10(-10) M to 10(-14) M or greater than 10(-8) M of somatostatin released significantly less amounts of TNF than did the untreated controls. TNF release by Kupffer cells treated with 10(-15) M to 10(-5) M of octreotide was significantly inhibited as compared to that of untreated controls. Kupffer cells treated with 10(-14) M to 10(-11) M and 10(-9) M to 10(-8) M of somatostatin released more H2O2 than did the untreated controls. The amount of H2O2 released by noncirrhotic Kupffer cells treated with 10(-6) M or 10(-5) M of somatostatin was less than that of controls. These findings demonstrate that somatostatin and octreotide modulate the release of nitric oxide, TNF, H2O be Kupffer cells depending on the concentration of hormones used.
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PMID:Somatostatin modulates the function of Kupffer cells. 922 98

In our previous studies we have shown that somatostatin and octreotide modulate the function of peritoneal macrophages and Kupffer cells in noncirrhotic livers. However, the effects of somatostatin on the Kupffer cells in cirrhotic livers are not known. In the present study, Kupffer cells, obtained from male rats with carbon tetrachloride-induced cirrhotic livers, were treated in vitro with somatostatin or octreotide and their effects on the release of nitric oxide, tumor necrosis factor-alpha (TNF-alpha) and peroxide (H2O2) determined. At concentrations of 10(-13) or 10(-10) to 10(-6) M of somatostatin or 10(-12) to 10(-10) M, or 10(-6) M of octreotide, the amount of nitric oxide released by Kupffer cells was significantly suppressed relative to that of untreated cells. Kupffer cells treated with less than 10(-12) M or greater than 10(-12) M of somatostatin or octreotide released less TNF-alpha compared to the untreated controls. In addition, zymosan-induced H2O2 release by Kupffer cells treated with 10(-9) to 10(-7) M somatostatin or with 10(-15) to 10(-13) M and 10(-9) to 10(-7) M of octreotide was greater than that of the untreated controls. These findings demonstrate that somatostatin and octreotide modulate the release of nitric oxide, TNF-alpha and H2O2 by Kupffer cells in cirrhotic livers depending on the concentrations of hormones used.
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PMID:Somatostatin and octreotide modulate the function of Kupffer cells in liver cirrhosis. 1010 Sep 24