Tissue Kallikrein Protects Rat Prostate against the Inflammatory Damage in a Chronic Autoimmune Prostatitis Model via Restoring Endothelial Function in a Bradykinin Receptor B2-Dependent Way.
Aged
Aged, 80 and over
Animals
Autoimmune Diseases
/ complications
Chronic Disease
Cytokines
/ metabolism
Disease Models, Animal
Endothelial Cells
/ metabolism
Humans
Hyperplasia
/ metabolism
Male
Middle Aged
Prostate
/ pathology
Prostatitis
/ complications
Protective Agents
/ administration & dosage
Rats
Rats, Wistar
Receptor, Bradykinin B2
/ metabolism
Retrospective Studies
Signal Transduction
/ drug effects
Tissue Kallikreins
/ administration & dosage
Journal
Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826
Informations de publication
Date de publication:
2022
2022
Historique:
received:
17
10
2021
revised:
13
01
2022
accepted:
18
01
2022
entrez:
14
2
2022
pubmed:
15
2
2022
medline:
19
3
2022
Statut:
epublish
Résumé
The aim of this study was to investigate whether tissue kallikrein (KLK1) can protect the prostate from inflammatory damage and the mechanism involved in it. A total of 50 male Wistar rats were used in this study. Initially, 20 rats were sacrificed to obtain the prostate antigen to induce experimental autoimmune prostatitis (EAP), and the remaining 30 rats were randomly divided into 5 experimental groups (normal control group (NC group), NC+KLK1 group (NCK group), EAP group, EAP+KLK1 group (EAPK group), and EAP+KLK1+HOE140 group (EAPKH group); The expression of KLK1 in the prostate decreased in the EAP group as well as BPH patients with obvious inflammation. KLK1 administration significantly inhibited inflammatory cell infiltration and reduced the production of inflammatory cytokines in the EAPK group. Prostate samples from the EAP group showed increased infiltration of T cells and macrophages, as well as gland atrophy, hypoxia, fibrosis, and angiogenesis. KLK1 administration upregulated endothelial nitric oxide synthase (eNOS) expression and suppressed oxidative stress, as well as transforming growth factor The KLK1 expression is inhibited in the inflamed prostates of humans and rats. Exogenous KLK1 restored endothelial function via a BDKRB2-dependent way and then played a role in improving microcirculation and exerted anti-inflammatory, antifibrotic, and antioxidative stress effects in the rat chronic-inflamed prostate.
Identifiants
pubmed: 35154561
doi: 10.1155/2022/1247806
pmc: PMC8826119
doi:
Substances chimiques
Cytokines
0
Protective Agents
0
Receptor, Bradykinin B2
0
Tissue Kallikreins
EC 3.4.21.35
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1247806Informations de copyright
Copyright © 2022 Mengyang Zhang et al.
Déclaration de conflit d'intérêts
All authors report no conflicts of interest.
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