Rhodiola crenulate alleviates hypobaric hypoxia-induced brain injury via adjusting NF-κB/NLRP3-mediated inflammation.
Adenosine Triphosphate
Animals
Antioxidants
/ metabolism
Brain Injuries
/ drug therapy
Caspase 1
Claudin-5
Hypoxia
/ drug therapy
Inflammation
/ metabolism
Interleukin-18
/ therapeutic use
Interleukin-6
Mice
NF-kappa B
/ metabolism
NLR Family, Pyrin Domain-Containing 3 Protein
/ metabolism
Rhodiola
Superoxide Dismutase
/ metabolism
Tumor Necrosis Factor-alpha
Energy metabolism
High-altitude hypoxic brain injury
NF-κB/NLRP3
Rhodiola crenulate
Journal
Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794
Informations de publication
Date de publication:
Aug 2022
Aug 2022
Historique:
received:
10
03
2022
revised:
15
05
2022
accepted:
02
06
2022
pubmed:
13
6
2022
medline:
24
6
2022
entrez:
12
6
2022
Statut:
ppublish
Résumé
Rhodiola crenulate (R. crenulate), a famous Tibetan medicine, has been demonstrated to possess superiorly protective effects in high-altitude hypoxic brain injury (HHBI). However, its mechanisms on HHBI are still largely unknown. Herein, the protective effects and underlying mechanisms of R. crenulate on HHBI of BABL/c mice were explored through in vivo experiments. The mice model of HHBI was established using an animal hypobaric and hypoxic chamber. R. crenulate extract (RCE) (0.5, 1.0 and 2.0 g/kg) was given by gavage for 7 days. Pathological changes and neuronal viability of mice hippocampus and cortex were evaluated using H&E and Nissl staining, respectively. The brain water content (BWC) in mice was determined by calculating the ratio of dry to wet weight of brain tissue. And serum of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH-Px) and lactate dehydrogenase (LDH) were detected via commercial biochemical kits. Synchronously, the contents of total antioxidant capacity (T-AOC), lactic acid (LA), adenosine triphosphate (ATP), succinate dehydrogenase (SDH), pyruvate kinase (PK), Ca The results demonstrated that RCE remarkably alleviated pathological damage, BWC, as well enhanced neuronal viability. Furthermore, the oxidative stress injuries were reversely abrogated after RCE treatment, evidenced by the increases of SOD, GSH-Px and T-AOC, while the decreases of MDA and LDH contents. Marvelously, the administration of RCE rectified and balanced the abnormal energy metabolism via elevating the levels of ATP, SDH, PK, Ca RCE may afford a protectively intervention in HHBI of mice through suppressing the oxidative stress, improving energy metabolism and the integrity of BBB, and subsiding inflammatory responses via the NF-κB/NLRP3 signaling pathway. As a promising agent for the treatment of mice HHBI, the deep-crossing molecular mechanisms of R. crenulate still needs to be further elucidated to identify novel core hub targets.
Sections du résumé
BACKGROUND
BACKGROUND
Rhodiola crenulate (R. crenulate), a famous Tibetan medicine, has been demonstrated to possess superiorly protective effects in high-altitude hypoxic brain injury (HHBI). However, its mechanisms on HHBI are still largely unknown.
METHODS
METHODS
Herein, the protective effects and underlying mechanisms of R. crenulate on HHBI of BABL/c mice were explored through in vivo experiments. The mice model of HHBI was established using an animal hypobaric and hypoxic chamber. R. crenulate extract (RCE) (0.5, 1.0 and 2.0 g/kg) was given by gavage for 7 days. Pathological changes and neuronal viability of mice hippocampus and cortex were evaluated using H&E and Nissl staining, respectively. The brain water content (BWC) in mice was determined by calculating the ratio of dry to wet weight of brain tissue. And serum of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH-Px) and lactate dehydrogenase (LDH) were detected via commercial biochemical kits. Synchronously, the contents of total antioxidant capacity (T-AOC), lactic acid (LA), adenosine triphosphate (ATP), succinate dehydrogenase (SDH), pyruvate kinase (PK), Ca
RESULTS
RESULTS
The results demonstrated that RCE remarkably alleviated pathological damage, BWC, as well enhanced neuronal viability. Furthermore, the oxidative stress injuries were reversely abrogated after RCE treatment, evidenced by the increases of SOD, GSH-Px and T-AOC, while the decreases of MDA and LDH contents. Marvelously, the administration of RCE rectified and balanced the abnormal energy metabolism via elevating the levels of ATP, SDH, PK, Ca
CONCLUSION
CONCLUSIONS
RCE may afford a protectively intervention in HHBI of mice through suppressing the oxidative stress, improving energy metabolism and the integrity of BBB, and subsiding inflammatory responses via the NF-κB/NLRP3 signaling pathway. As a promising agent for the treatment of mice HHBI, the deep-crossing molecular mechanisms of R. crenulate still needs to be further elucidated to identify novel core hub targets.
Identifiants
pubmed: 35691080
pii: S0944-7113(22)00319-1
doi: 10.1016/j.phymed.2022.154240
pii:
doi:
Substances chimiques
Antioxidants
0
Claudin-5
0
Interleukin-18
0
Interleukin-6
0
NF-kappa B
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Nlrp3 protein, mouse
0
Tumor Necrosis Factor-alpha
0
Adenosine Triphosphate
8L70Q75FXE
Superoxide Dismutase
EC 1.15.1.1
Caspase 1
EC 3.4.22.36
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
154240Informations de copyright
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