Experimental study on the antiviral mechanism of Ceratostigma willmattianum against herpes simplex virus type 1 in vitro.
- Author:
Tian CHEN
1
;
Wen-xiang JIA
;
Fa-long YANG
;
Yi XIE
;
Wei-qing YANG
;
Wei ZENG
;
Zai-rong ZHANG
;
Hui LI
;
Si-ping JIANG
;
Zhen YANG
;
Jin-rui CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antiviral Agents; pharmacology; Cell Adhesion; Cercopithecus aethiops; DNA Replication; drug effects; Dose-Response Relationship, Drug; Drugs, Chinese Herbal; administration & dosage; isolation & purification; pharmacology; Glycoproteins; biosynthesis; genetics; Herpesvirus 1, Human; drug effects; physiology; Plants, Medicinal; chemistry; Primulaceae; chemistry; RNA, Messenger; biosynthesis; genetics; Vero Cells; drug effects; virology; Virus Replication; drug effects
- From: China Journal of Chinese Materia Medica 2004;29(9):882-886
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the antiviral effect and mechanisms of the liquid extract from Ceratostigma willmattianum against herpes simplex virus type 1 (HSV-1) in vitro.
METHODC. willmattianum in various concentration was applied to different steps of HSV-1 replication cycle. 50% Tissue culture infective dose (TCID50), cytopathic effect (CPE), MTT staining method, dot blotting and Northern blotting analysis were used to estimate index of antiviral activity.
RESULT50% Toxic concentration (TC50) was 1077 mg x L(-1), IC50 29.46 mg x L(-1) and therapeutic index (TI) 36.56 in C. willmattianum. TC50 330 mg x L(-1), 50% Inhibiting concentration (IC50) 9.12 mg x L(-1) and TI 36.18 in ACV by MTT staining method. The liquid extract from C. willmattianum had remarkable effect on inhibiting HSV-1 in vitro. Ceratostigma could interfere absorption of HSV-1 to Vero cells to prevent HSV-1 infectivity, inhibit HSV-1 gD DNA replication and HSV-1 gD mRNA expression.
CONCLUSIONC. willmattianum possesses strong anti-HSV-1 activity in vitro. The antiviral mechanisms are related to inhibiting virus absorption, HSV-1 gD gene replication and HSV-1 gD gene transcription.
