α-adrenoblockers modulatory effect on the noise-mediated several biochemical and morpho-immuno-histochemical changes in the rat's blood plasma and tissues.

Experimental studies of chronic noise exposure in modern urban life testified about oxidative stress due to the corresponding hormones effects leading to accumulation of reactive oxygen species and endothelial dysfunction. This study aims to evaluate the protective effect of α2-adrenoblockers to modulate oxidative stress and corticosterone levels due to chronic noise exposure. To achieve this, we examined the effects of beditin (2-aminothiozolyl-1,4-benzodioxane) and mesedin (2-(2-methyl-amino-thiozolyl)-1,4-benzodioxane hydrochloride), along with changes in corticosterone, Ca2 + content, and morphological alterations in various tissues under noise-induced stress.

Morpho‑functional study of the hypothalamic proline‑rich polypeptide apoptotic activity against mouse Ehrlich ascites carcinoma.

A new type of bioactive polypeptides of the neurosecretory hypothalamus called proline‑rich peptides (PRPs), which are isolated from bovine neurosecretory granules of the neurohypophysis, are synthesized in the form of a common precursor protein (neurophysin vasopressin‑associated glycoprotein). Proline‑rich polypetide 1 (PRP‑1; also known as galarmin) is comprised of 15 amino acids residues, and has been suggested to possess anti‑neurodegenerative, immunoregulatory, hematopoietic, antimicrobial and antitumor properties. The cytostatic, antiproliferative effect of PRP‑1 was demonstrated in the human chondrosarcoma JJ012 and triple negative breast carcinoma MDA MB 231 cell lines.

Toll like receptors TLR1/2, TLR6 and MUC5B as binding interaction partners with cytostatic proline rich polypeptide 1 in human chondrosarcoma.

Metastatic chondrosarcoma is a bone malignancy not responsive to conventional therapies; new approaches and therapies are urgently needed. We have previously reported that mTORC1 inhibitor, antitumorigenic cytostatic proline rich polypeptide 1 (PRP-1), galarmin caused a significant upregulation of tumor suppressors including TET1/2 and SOCS3 (known to be involved in inflammatory processes), downregulation of oncoproteins and embryonic stem cell marker miR-302C and its targets Nanog, c-Myc and Bmi-1 in human chondrosarcoma. To understand better the mechanism of PRP-1 action it was very important to identify the receptor it binds to.