Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.24.23 (
MMP
)
4,246
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A salt tolerant plant, Corydalis heterocarpa has been used as a folk medicine to treat travail and spasm. Recent studies have also reported antioxidant and antiinflammatory activities of compounds isolated from C. heterocarpa. In this study, the protective effect of (2'S)-columbianetin isolated from C. heterocarpa on UVB-induced human keratinocyte (HaCaT) damage was investigated. First, the appropriate energy level of UVB irradiation was determined using MTT and LDH assays. And then the protective effect of (2'S)-columbianetin on UVB induced HaCaT damage was evaluated by measuring; the changes in cell viability, LDH release level, ROS generation, cell cycle arrest and
MMP
expression levels. Finally, the effect of compound on MAPK and AP-1 signaling pathways were studied to understand the underlying signaling mechanisms. Result demonstrated that the presence of (2'S)-columbianetin suppressed the reactive oxygen species (ROS) generation, cell cycle arrest at sub-G1 phase and down regulation of
MMP
expression in UVB treated HaCaT cells. Furthermore, stress activated signaling pathways (
ASK1
-MAPK) and AP-1 signaling pathway were regulated by (2'S)-columbianetin treatment. These results suggest that (2'S)-columbianetin could be effectively used to protect human keratinocytes from UVB induced damage.
...
PMID:Protective effect of (2'S)-columbianetin from Corydalis heterocarpa on UVB-induced keratinocyte damage. 2232 94
Ultraviolet-B (UVB) irradiation acts primarily on the epidermal basal cell layer of the skin, inducing harmful biological effects. In this study, we have investigated the effect of libanoridin isolated from Corydalis heterocarpa against UVB-induced damage in human keratinocyte (HaCaT) cells and the molecular mechanism underlying those effects. Treatment with libanoridin inhibited the cell cytotoxicity and LDH induced by UVB exposure at 40 mJ/cm(2). Additionally, expression levels of type IV collagenases (MMP-2, MMP-9) were decreased by libanoridin. Furthermore,
MMP
tissue inhibitors were enhanced followed by treatment with libanoridin. Moreover, UVB-induced activation of phosphorylation of three MAPKs such as JNK, ERK, p38 and AP-1 transcription factor were decreased by treatment with libanoridin. Our present study demonstrates that libanoridin has the abilities to inhibit UVB-induced cellular damage via
ASK1
-MAPK and AP-1 signalling pathways. Therefore, libanoridin may be used as an effective natural compound to prevent skin damage due to UVB exposure.
...
PMID:Photoprotective effect of libanoridin isolated from Corydalis heterocarpa on UVB stressed human keratinocyte cells. 2336 77
In this study, total flavonoids and total triterpenoid acid were extracted with ethyl acetate from Hedyotis diffusa Willd, and hepatoprotective activities of them and five compounds from total flavonoids against H
2
O
2
induced hepatocyte damage on HL-02 cells were determined. In particular, amentoflavone and total flavonoids had influence on the leakage of ALT, AST, LDH, the activities of SOD and the content of MDA. They effectively reduced the loss of
MMP
, the release of Cyt C, and then inhibited activation of caspase-3/caspase-9 cascade in hepatotoxic cells. The contents of ROS were significantly reduced to inhibit p38 in amentoflavone and flavonoids groups which decreased
ASK1
and p-p38 levels through increasing thioredoxin Trx1 and reductase TrxR1. These results suggesting that the antioxidant protection of amentoflavone and flavonoids might be reducing ROS to inhibit the H
2
O
2
-induced upstream of pathway via increasing levels of Trx1 and TrxR1, which were pivotal in blocking the down streaming effectors of
ASK1
/p38 MAPK pathway and alleviating hepatotoxicity.
...
PMID:Protective Antioxidant Effects of Amentoflavone and Total Flavonoids from Hedyotis diffusa on H
2
O
2
-Induced HL-O2 Cells through ASK1/p38 MAPK Pathway. 3234 91