Effects of Baicalin on piglet monocytes involving PKC-MAPK signaling pathways induced by Haemophilus parasuis.
Animals
Animals, Newborn
/ metabolism
Anti-Bacterial Agents
/ pharmacology
Apoptosis
/ drug effects
Dose-Response Relationship, Drug
Flavonoids
/ pharmacology
Haemophilus Infections
/ drug therapy
Haemophilus parasuis
/ drug effects
MAP Kinase Signaling System
/ drug effects
Monocytes
/ drug effects
Reactive Oxygen Species
/ metabolism
Swine
Swine Diseases
/ drug therapy
Apoptosis
Baicalin
Glässer’s disease
Haemophilus parasuis
PKC–MAPK
Journal
BMC veterinary research
ISSN: 1746-6148
Titre abrégé: BMC Vet Res
Pays: England
ID NLM: 101249759
Informations de publication
Date de publication:
25 Mar 2019
25 Mar 2019
Historique:
received:
19
01
2018
accepted:
07
03
2019
entrez:
27
3
2019
pubmed:
27
3
2019
medline:
30
4
2019
Statut:
epublish
Résumé
Haemophilus parasuis (HPS) is the causative agent of Glässer's disease, characterized by arthritis, fibrinous polyserositis and meningitis, and resulting in worldwide economic losses in the swine industry. Baicalin (BA), a commonly used traditional Chinese medication, has been shown to possess a series of activities, such as anti-bacterial, anti-viral, anti-tumor, anti-oxidant and anti-inflammatory activities. However, whether BA has anti-apoptotic effects following HPS infection is unclear. Here, we investigated the anti-apoptotic effects and mechanisms of BA in HPS-induced apoptosis via the protein kinase C (PKC)-mitogen-activated protein kinase (MAPK) pathway in piglet's mononuclear phagocytes (PMNP). Our data demonstrated that HPS could induce reactive oxygen species (ROS) production, arrest the cell cycle and promote apoptosis via the PKC-MAPK signaling pathway in PMNP. Moreover, when BA was administered, we observed a reduction in ROS production, suppression of cleavage of caspase-3 in inducing apoptosis, and inhibition of activation of the PKC-MAPK signaling pathway for down-regulating p-JNK, p-p38, p-ERK, p-PKC-α and PKC-δ in PMNP triggered by HPS. Our data strongly suggest that BA can reverse the apoptosis initiated by HPS through regulating the PKC-MAPK signaling pathway, which represents a promising therapeutic agent in the treatment of HPS infection.
Sections du résumé
BACKGROUND
BACKGROUND
Haemophilus parasuis (HPS) is the causative agent of Glässer's disease, characterized by arthritis, fibrinous polyserositis and meningitis, and resulting in worldwide economic losses in the swine industry. Baicalin (BA), a commonly used traditional Chinese medication, has been shown to possess a series of activities, such as anti-bacterial, anti-viral, anti-tumor, anti-oxidant and anti-inflammatory activities. However, whether BA has anti-apoptotic effects following HPS infection is unclear. Here, we investigated the anti-apoptotic effects and mechanisms of BA in HPS-induced apoptosis via the protein kinase C (PKC)-mitogen-activated protein kinase (MAPK) pathway in piglet's mononuclear phagocytes (PMNP).
RESULTS
RESULTS
Our data demonstrated that HPS could induce reactive oxygen species (ROS) production, arrest the cell cycle and promote apoptosis via the PKC-MAPK signaling pathway in PMNP. Moreover, when BA was administered, we observed a reduction in ROS production, suppression of cleavage of caspase-3 in inducing apoptosis, and inhibition of activation of the PKC-MAPK signaling pathway for down-regulating p-JNK, p-p38, p-ERK, p-PKC-α and PKC-δ in PMNP triggered by HPS.
CONCLUSIONS
CONCLUSIONS
Our data strongly suggest that BA can reverse the apoptosis initiated by HPS through regulating the PKC-MAPK signaling pathway, which represents a promising therapeutic agent in the treatment of HPS infection.
Identifiants
pubmed: 30909903
doi: 10.1186/s12917-019-1840-x
pii: 10.1186/s12917-019-1840-x
pmc: PMC6434632
doi:
Substances chimiques
Anti-Bacterial Agents
0
Flavonoids
0
Reactive Oxygen Species
0
baicalin
347Q89U4M5
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
98Subventions
Organisme : National Natural Science Foundation of China
ID : 31572572
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