Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the effect and mechanism of NK-1 Tachykinin receptor (NK-IR) antagonist on hypoxia induced hepatic injury, we established the hypoxic rat model. 30 male SD rats (weighing 240-300g) were randomly divided into 3 groups, control group, and experimental groups including the hypoxia group and the NK-1R antagonist group. The rats of experimental groups underwent hypoxia, among them the NK-1R antagonist group were those with interference of NK-1R antagonist by intraperitoneal injection. Hepatic injury was evaluated by pathological staining, hepatic function detection and hepatocellular apoptosis determination. Results showed hypoxia-induced hepatic injury in rats was established successfully. Edema,ballooning degeneration and spotty necrosis were found in livers in the experimental groups, among which the pathological injury in the hypoxia group was worse than that in the NK-1R antagonist group. Moreover,GGT and the rate of hepatocellular apoptosis in the NK-1R antagonist group were obviously lower than that in the hypoxia group (P<0.05). But no significant difference were found in ALT,AST and ALP between groups (P>0.05). These data indicate that Substance P possibly participate in the process of hypoxia-induced hepatic injury, and NK-1R antagonist could reduce hypoxia-induced hepatic injury.
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PMID:[The effect of NK-1 tachykinin receptor antagonist on hypoxia induced hepatic function injury and hepatocellular apoptosis in rats]. 2209 70

Neuropeptides released from the skeletal nerve fibers have neurotransmitter and immunoregulatory roles; they exert paracrine biological effects on bone cells present close to the nerve endings expressing these signaling molecules. The aims of this study were a systematic investigation of the effects of the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), Neuropeptide Y (NPY) and tyrosine hydroxylase (TH) on the cell viability and function of the human osteoblasts, and comparing their difference in the role of regulating bone formation. Cultures of normal human osteoblasts were treated with SP, CGRP, VIP, NPY or TH at three concentrations. We found that each of the five neuropeptides induced increases in cell viability of human osteoblasts. The stimulatory action of NPY was the highest, followed by VIP, SP and TH, while CGRP had the lowest stimulatory effect. The viability index of osteoblasts was inversely associated with the concentration of neuropeptides, and positively with the time of exposure. Moreover, the five neuropeptides increased the ALP activity and osteocalcin to different extents in a dose-dependent manner. The GJIC of osteoblasts was significantly promoted by neuropeptides. The results demonstrated that neuropeptides released from skeletal nerve endings after a stimulus appeared to be able to induce the proliferation and activity of osteoblasts via enhancing GJIC between cells, and further influence the bone formation. These findings may contribute toward a better understanding of the neural influence on bone remodeling and improving treatments related to bone diseases.
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PMID:Neuropeptides stimulate human osteoblast activity and promote gap junctional intercellular communication. 2372 61

Clinical observations suggest neuronal control of bone remodeling. Sensory nerve fibers innervating bone, bone marrow and periosteum signal via neurotransmitters including substance P (SP). In previous studies we observed impaired biomechanical and structural bone parameters in tachykinin (Tac) 1-deficient mice lacking SP. Here, we aim to specify effects of SP on metabolic parameters of bone marrow macrophage (BMM)/osteoclast cultures and osteoblasts isolated from Tac1-deficient and wildtype (WT) mice. We demonstrated endogenous SP production and secretion in WT bone cells. Absence of SP reduced bone resorption rate, as we found reduced numbers of precursor cells (BMM) and multinucleated osteoclasts and measured reduced cathepsin K activity in Tac1-/- BMM/osteoclast cultures. However, this might partly be compensated by reduced apoptosis rate and increased fusion potential of Tac1-/- precursor cells to enlarged "super" osteoclasts. Contrarily, increased ALP enzyme activity and apoptosis rate during early osteoblast differentiation accelerated osteogenesis and cell death in the absence of SP together with reduced ALP activity of Tac1-/- osteoblasts during late osteogenic differentiation resulting in reduced bone formation at later stages. Therefore, we suggest that absence of SP presumably results in a slight reduction of bone resorption rate but concomitantly in a critical reduction of bone formation and mineralization rate.
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PMID:Substance P modulates bone remodeling properties of murine osteoblasts and osteoclasts. 2990 30