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Drug-Target Interaction

Drug

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PubChem ID:197810
Structure:
Synonyms:
(+)-chelidonine
(5bR,6S,12bS)-
476-32-4
5b,6,7,12b,13,14-Hexahydro-13-methyl[1,3]benzodioxolo[5,6-c]-1,3-dioxolo[4
5b,6,7,12b,13,14-Hexahydro-13-methyl[1,3]benzodioxolo[5,6-c]-1,3-dioxolo[4,5-i]phenan-thridin-6-ol;[1,3]Benzodioxolo[5,6-c]-1,3-dioxolo[4,5-i]phenanthridin-6-ol, 5b,6,7,12b,13,14-hexahydro-13-methyl-, (5bR,6S,12bS)-
AC1L542Q
ACon1_000007
AIDS-002651
AIDS002651
Benzophenanthridine alkaloid
BPBio1_000478
BRD-K32828673-001-01-5
BRD-K32828673-002-03-9
BSPBio_000434
C12242
CHEBI:31389
Chelidonin
Chelidonine
CHEMBL496867
Helidonine
Khelidonin
MEGxp0_001421
NCGC00167959-01
NCGC00167959-02
NCGC00167959-03
NP-006299
NSC646661
NSC646661 (FREE BASE)
Prestwick0_000587
Prestwick1_000587
Prestwick2_000587
Prestwick3_000587
SPBio_002653
Stylophorin
ZINC30727894

Target

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Uniprot ID:Q6P9U7_RAT
Synonyms:
L-lactate dehydrogenase
EC-Numbers:1.1.1.27
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

10603424
Protein kinase C inhibitors abolish the increased resistance of diabetic rat heart to ischemia-reperfusion injury.. C H Moon; Y S Jung; S H Lee; E J Baik (1999) The Japanese journal of physiology display abstract
Protein kinase C (PKC) has been implicated in ischemic preconditioning, but whether it plays a role in the cardioprotection observed in the diabetic heart is not known. We assessed the possible role of PKC by investigating whether the inhibition of PKC with staurosporine (Stau, 0.01 microM) or chelerythrine (Chel, 1 microM) can abolish the increased resistance to ischemia (25 min)-reperfusion (30 min) injury in Langendorff perfused hearts from streptozotocin-induced 4-week diabetic rats. In the diabetic heart, pre-ischemic left ventricular developed pressure (LVDP), double product (DP: LVDPxheart rate/1,000), +/- dP/dt(max) and coronary flow rate (CFR) were all reduced compared to the control. The pretreatment with Stau or Chel significantly improved these parameters. The post-ischemic contractile function was recovered to a greater extent in the diabetic heart (116.9 +/- 20.5% of pre-ischemic DP) than in the control (23.3 +/- 2.3% of pre-ischemic DP), indicating the increased resistance of the diabetic heart to ischemia-reperfusion injury. The treatment with Stau or Chel abolished the enhanced recovery in the diabetic heart (36.0 +/- 14.6 and 54.1 +/- 12.8% of pre-ischemic DP, respectively). The reduction in post-ischemic end diastolic pressure (EDP) and lactate dehydrogenase (LDH) release in diabetes (13.5 +/- 2.5 mmHg and 27.2 +/- 6.2 U/g heart) compared to the control (55.8 +/- 2.9 mmHg and 60. 3 +/- 5.7 U/g heart) was significantly (p