PMID- 36774389
OWN - NLM
STAT- MEDLINE
DCOM- 20230214
LR  - 20230320
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 13
IP  - 1
DP  - 2023 Feb 11
TI  - Mechanism of arterial injury exacerbated by hyperhomocysteinemia in spontaneously 
      hypertensive rats.
PG  - 2482
LID - 10.1038/s41598-023-28731-9 [doi]
LID - 2482
AB  - Hypertension associated with hyperhomocysteinemia (HHcy) accounts for 75% of 
      hypertension in China. HHcy plays a synergistic role with hypertension in 
      vascular injury and significantly increases the incidence of cardiovascular and 
      cerebrovascular diseases. The present study aimed to explore the molecular 
      mechanism of HHcy-induced arterial injury in hypertension. Spontaneously 
      hypertensive rats (SHR) were injected intraperitoneally with DL-homocysteine 
      (Hcy) to construct the model of hypertension associated with HHcy (HHcy + SHR). 
      Biological network was employed to identify the material basis of arterial injury 
      in hypertension associated with HHcy. The prediction molecules in oxidative 
      stress and inflammation pathways were experimentally verified by quantitative 
      real-time polymerase chain reaction (qRT-PCR) and western blot (WB) analysis. The 
      HHcy + SHR group significantly increased oxidative stress pathway molecules: 
      nicotinamide adenine dinucleotide phosphate oxidase (Nox); inflammatory pathway 
      molecules: vascular adhesion protein-1 (VAP-1), interleukin-6 (IL-6) and tumor 
      necrosis factor-alpha (TNF-a); as well as inflammatory pathway regulatory 
      factors: nuclear factor-kappa-gene binding (NF-kappaB) p65 and protein kinase B (Akt1). 
      Among them, IL-6 was also significantly increased in the HHcy group. Both 
      oxidative stress and inflammation contributed to the arterial injury of 
      hypertension associated with HHcy, and inflammation mechanism might play a 
      leading role in HHcy aggravating arterial injury, at least partially through the 
      Akt1/NF-kappaB p65/IL-6 signaling pathway.
CI  - (c) 2023. The Author(s).
FAU - Zhang, Lihua
AU  - Zhang L
AD  - Department of Medicine, Jinan Maternity and Child Care Hospital Affiliated to 
      Shandong First Medical University, Jinan, China.
FAU - Xu, Rui
AU  - Xu R
AD  - Department of Cardiology, Central Hospital Affiliated to Shandong First Medical 
      University, Jinan, 250013, Shandong, People's Republic of China. 
      xuruicn@hotmail.com.
FAU - Ma, Xiaoshan
AU  - Ma X
AD  - Department of Medicine, Jinan Maternity and Child Care Hospital Affiliated to 
      Shandong First Medical University, Jinan, China.
FAU - Zhang, Xia
AU  - Zhang X
AD  - Laboratory Department, Jinan Maternity and Child Care Hospital, Jinan, China.
FAU - Gong, Jun
AU  - Gong J
AD  - Department of Women Healthcare, Jinan Maternity and Child Care Hospital 
      Affiliated to Shandong First Medical University, Jinan, China.
FAU - Li, Zhongliang
AU  - Li Z
AD  - Department of Women Healthcare, Jinan Maternity and Child Care Hospital 
      Affiliated to Shandong First Medical University, Jinan, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230211
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (NF-kappa B)
RN  - 0 (Interleukin-6)
RN  - 0LVT1QZ0BA (Homocysteine)
SB  - IM
MH  - Rats
MH  - Animals
MH  - Rats, Inbred SHR
MH  - NF-kappa B/metabolism
MH  - Interleukin-6/genetics
MH  - *Hyperhomocysteinemia/complications
MH  - *Vascular System Injuries/complications
MH  - Inflammation/metabolism
MH  - *Hypertension/complications
MH  - Homocysteine
PMC - PMC9922276
COIS- The authors declare no competing interests.
EDAT- 2023/02/12 06:00
MHDA- 2023/02/15 06:00
PMCR- 2023/02/11
CRDT- 2023/02/11 23:25
PHST- 2022/03/15 00:00 [received]
PHST- 2023/01/24 00:00 [accepted]
PHST- 2023/02/11 23:25 [entrez]
PHST- 2023/02/12 06:00 [pubmed]
PHST- 2023/02/15 06:00 [medline]
PHST- 2023/02/11 00:00 [pmc-release]
AID - 10.1038/s41598-023-28731-9 [pii]
AID - 28731 [pii]
AID - 10.1038/s41598-023-28731-9 [doi]
PST - epublish
SO  - Sci Rep. 2023 Feb 11;13(1):2482. doi: 10.1038/s41598-023-28731-9.