PMID- 38058079
OWN - NLM
STAT- MEDLINE
DCOM- 20231211
LR  - 20231211
IS  - 1944-7930 (Electronic)
IS  - 1539-6509 (Linking)
VI  - 35
IP  - 179
DP  - 2023 Dec
TI  - Eriocitrin Alleviates Inflammation and Oxidative Stress in Subarachnoid 
      Hemorrhage by Regulating DUSP14.
PG  - 1134-1146
LID - 10.24976/Discov.Med.202335179.110 [doi]
AB  - BACKGROUND: Inflammation and oxidative stress (OS) are major causes of aneurysmal 
      subarachnoid hemorrhage (aSAH)-induced early brain injury (EBI). Eriocitrin (EC), 
      a flavonoid compound, has anti-inflammatory and antioxidant actions. However, 
      there is still no relevant studies on the role of EC in SAH. Accordingly, this 
      research aims to clarify the anti-OS and anti-inflammatory efficacy of EC in SAH. 
      METHOD: Rat SAH model was established in vivo and administered with Eriocitrin 
      (25 mg/kg). In vitro, BV2 cells were exposed to oxyhemoglobin (OxyHb) for 24 
      hours and pretreated with Eriocitrin (1 uM/mL, 2 uM/mL, 4 uM/mL) for 30 minutes. 
      Water maze experiments and neurological function scores were conducted to assess 
      cognitive and motor function. TdT-mediated dUTP Nick-End Labeling (TUNEL) 
      staining was used to detect cortical cell apoptosis. Enzyme-linked immunosorbent 
      assay (ELISA) and polymerase chain reaction (PCR) were used to detect the 
      inflammatory factors and malondialdehyde (MDA), as well as the expression of 
      superoxide dismutase (SOD) and glutathione peroxidase (GSH-px). Western blots 
      were used to semi quantify nuclear factor erythroid-2-related factor 2 (Nrf2), 
      nuclear factor-kappaB (NF-kappaB), dual specificity phosphatase 14 (DUSP14) expression. 
      RESULTS: The findings suggest that EC (25 mg/kg) reduced SAH-induced central 
      nervous system (CNS) damage, neuronal apoptosis, inflammatory reactions and OS. 
      Regarding a mechanistic study, EC enhanced Nrf2 and NF-kappaB by increasing DUSP14 
      activation, thereby reducing the inflammatory cytokines interleukin (IL)-1beta, 
      tumor necrosis factor (TNF)-alpha, and IL-6. In addition, EC decreased MDA while 
      markedly elevating SOD and enhancing GSH-px. Furthermore, specifically inhibiting 
      DUSP14 expression via using protein-tyrosine-phosphatase (PTP) inhibitor IV, 
      neutralized the protective action of EC and aggravated inflammation and OS. In 
      vitro experiments of OxyHb-induced BV2 cells revealed that EC promoted Nrf2 while 
      markedly suppressing NF-kappaB by increasing DUSP14 activation, thereby reducing the 
      concentrations of the above inflammatory cytokines. Moreover, EC decreased MDA 
      while evidently increasing SOD and GSH-px. CONCLUSION: In summary, this paper 
      lays a theoretical grounding for EC treatment of SAH-induced inflammatory 
      reactions and OS by regulating DUSP14.
FAU - Sheng, Liuqing
AU  - Sheng L
AD  - Department of Neurosurgery, Renmin Hospital of Wuhan University, 430060 Wuhan, 
      Hubei, China.
AD  - Department of Neurosurgery, The Third People's Hospital of Hubei Province, 430014 
      Wuhan, Hubei, China.
FAU - Yao, Xiaolong
AU  - Yao X
AD  - Department of Neurosurgery, The Third People's Hospital of Hubei Province, 430014 
      Wuhan, Hubei, China.
FAU - Ye, Jianfeng
AU  - Ye J
AD  - Department of Neurosurgery, The Third People's Hospital of Hubei Province, 430014 
      Wuhan, Hubei, China.
FAU - Wang, Zhizhong
AU  - Wang Z
AD  - Department of Neurosurgery, The Third People's Hospital of Hubei Province, 430014 
      Wuhan, Hubei, China.
FAU - Chen, Yinchun
AU  - Chen Y
AD  - Department of Neurosurgery, The Third People's Hospital of Hubei Province, 430014 
      Wuhan, Hubei, China.
FAU - Li, Jun
AU  - Li J
AD  - Department of Neurosurgery, The Third People's Hospital of Hubei Province, 430014 
      Wuhan, Hubei, China.
FAU - Li, Mingchang
AU  - Li M
AD  - Department of Neurosurgery, Renmin Hospital of Wuhan University, 430060 Wuhan, 
      Hubei, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Discov Med
JT  - Discovery medicine
JID - 101250006
RN  - 0 (NF-kappa B)
RN  - AS293HR5XQ (eriocitrin)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Rats
MH  - Animals
MH  - *NF-kappa B/metabolism/pharmacology/therapeutic use
MH  - *Subarachnoid Hemorrhage/complications/drug therapy/pathology
MH  - NF-E2-Related Factor 2/metabolism/pharmacology/therapeutic use
MH  - Rats, Sprague-Dawley
MH  - Oxidative Stress
MH  - Inflammation/drug therapy/pathology
MH  - Anti-Inflammatory Agents/pharmacology/therapeutic use
MH  - Cytokines/metabolism
MH  - Superoxide Dismutase/metabolism/pharmacology/therapeutic use
OTO - NOTNLM
OT  - DUSP14
OT  - NF-kappaB
OT  - SAH
OT  - eriodocitrin
OT  - inflammatory
OT  - oxidative stress
EDAT- 2023/12/07 06:42
MHDA- 2023/12/11 12:43
CRDT- 2023/12/07 01:13
PHST- 2023/12/11 12:43 [medline]
PHST- 2023/12/07 06:42 [pubmed]
PHST- 2023/12/07 01:13 [entrez]
AID - 1701411457150-439657466 [pii]
AID - 10.24976/Discov.Med.202335179.110 [doi]
PST - ppublish
SO  - Discov Med. 2023 Dec;35(179):1134-1146. doi: 10.24976/Discov.Med.202335179.110.