[병리학 논문분석] PDL cell과 LPS와 nicotine 처리했을때의 VEGF 발현에 관한 연구에 대한 자료입니다.
1. Effects of nicotine and lipopolysaccharide on periodontal ligament
2) VEGF up-regulation & down-regulation
4. MMP series
5. VEGF signaling Pathway
Lipopolysaccharides (LPS), also known as lipoglycans,
are large molecules consisting of a lipid and a polysaccharide
joined by a covalent bond; they are found in the outer
membrane of Gram-negative bacteria, act as endotoxins and
elicit strong immune responses in animals.
LPS is the major component of the outer membrane of
Gram-negative bacteria, contributing greatly to the structural
integrity of the bacteria, and protecting the membrane
from certain kinds of chemical attack. LPS also increases
the negative charge of the cell membrane and helps
stabilize the overall membrane structure. It is of crucial
importance to gram-negative bacteria, whose death results
if it is mutated or removed. LPS is an endotoxin, and induces
a strong response from normal animal immune systems.
Hypothesized mechanism of cigarette smoke-induced proinflammatory mediator release via sirtuin-NF-κB RelA/p65 interaction. Cigarette smoke decreased sirtuin levels and caused posttranslational modification by reactive aldehydes/reactive oxygen species/RNS, thereby disrupting SIRT1-RelA/p65 complex via phosphorylation (P) and acetylation (Ac) of RelA/p65. This leads to increased release of pro-inflammatory mediators. RNS, reactive nitrogen species.