PMID- 36798091
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230218
IS  - 2049-9442 (Electronic)
IS  - 2049-9434 (Print)
IS  - 2049-9434 (Linking)
VI  - 18
IP  - 3
DP  - 2023 Mar
TI  - Pinostrobin alleviates chronic restraint stress‑induced cognitive impairment by 
      modulating oxidative stress and the function of astrocytes in the hippocampus of 
      rats.
PG  - 20
LID - 10.3892/br.2023.1602 [doi]
LID - 20
AB  - Chronic stress has been recognized to induce the alterations of neuronal and 
      glial cells in the hippocampus, and is thus implicated in cognitive dysfunction. 
      There is increasing evidence to indicate that natural compounds capable of 
      exerting neuroprotective and antioxidant activities, may function as potential 
      therapeutic agents for cognitive impairment. The present study examined the 
      neuroprotective effects of pinostrobin from Boesenbergia rotunda (L.) against 
      chronic restraint stress (CRS)-induced cognitive impairment associated with the 
      alterations of oxidative stress, neuronal density and glial fibrillary acidic 
      protein (GFAP) of astrocytes in the hippocampus. For this purpose, male Wistar 
      rats were administered once daily with pinostrobin (20 and 40 mg/kg, per os) 
      prior to exposure to CRS (6 h/day) for 21 days. The cognitive behaviors, the 
      concentration of malondialdehyde, and the activities of superoxide dismutase and 
      catalase were determined. Histologically, the alterations in astrocytic GFAP and 
      excitatory amino acid transporter 2 (EAAT2) in the hippocampus were examined. The 
      results revealed that pinostrobin potentially attenuated cognitive impairment in 
      the Y-maze and in novel object recognition tests, with a reduction in oxidative 
      stress. Furthermore, pinostrobin effectively increased neuronal density, as well 
      as the immunoreactivities of GFAP and EAAT2 in the hippocampus. Taken together, 
      these findings indicate that treatment with pinostrobin alleviates chronic 
      stress-induced cognitive impairment by exerting antioxidant effects, reducing 
      neuronal cell damage, and improving the function of astrocytic GFAP and EAAT2. 
      Thus, pinostrobin may have potential for use as a neuroprotective agent to 
      protect against chronic stress-induced brain dysfunction and cognitive deficits.
CI  - Copyright: (c) Thongrong et al.
FAU - Thongrong, Sitthisak
AU  - Thongrong S
AD  - Division of Anatomy, School of Medical Sciences, University of Phayao, Phayao 
      56000, Thailand.
AD  - Unit of Excellence in Translational Neurosciences Initiative, University of 
      Phayao, Phayao 56000, Thailand.
FAU - Surapinit, Serm
AU  - Surapinit S
AD  - Unit of Excellence in Translational Neurosciences Initiative, University of 
      Phayao, Phayao 56000, Thailand.
AD  - Department of Medical Technology, School of Allied Health Sciences, University of 
      Phayao, Phayao 56000, Thailand.
FAU - Promsrisuk, Tichanon
AU  - Promsrisuk T
AD  - Division of Physiology, School of Medical Sciences, University of Phayao, Phayao 
      56000, Thailand.
FAU - Jittiwat, Jinatta
AU  - Jittiwat J
AD  - Faculty of Medicine, Mahasarakham University, Mahasarakham 44000, Thailand.
FAU - Kongsui, Ratchaniporn
AU  - Kongsui R
AD  - Unit of Excellence in Translational Neurosciences Initiative, University of 
      Phayao, Phayao 56000, Thailand.
AD  - Division of Physiology, School of Medical Sciences, University of Phayao, Phayao 
      56000, Thailand.
LA  - eng
PT  - Journal Article
DEP - 20230202
PL  - England
TA  - Biomed Rep
JT  - Biomedical reports
JID - 101613227
PMC - PMC9922797
OTO - NOTNLM
OT  - astrocytes
OT  - chronic restraint stress
OT  - cognitive impairment
OT  - hippocampus
OT  - oxidative stress
OT  - pinostrobin
COIS- The authors declare that they have no competing interests.
EDAT- 2023/02/18 06:00
MHDA- 2023/02/18 06:01
PMCR- 2023/02/02
CRDT- 2023/02/17 02:04
PHST- 2022/11/19 00:00 [received]
PHST- 2023/01/27 00:00 [accepted]
PHST- 2023/02/17 02:04 [entrez]
PHST- 2023/02/18 06:00 [pubmed]
PHST- 2023/02/18 06:01 [medline]
PHST- 2023/02/02 00:00 [pmc-release]
AID - BR-18-3-01602 [pii]
AID - 10.3892/br.2023.1602 [doi]
PST - epublish
SO  - Biomed Rep. 2023 Feb 2;18(3):20. doi: 10.3892/br.2023.1602. eCollection 2023 Mar.