2022
DOI: 10.1016/j.jss.2021.12.013
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Electroacupuncture Relieves Hippocampal Injury by Heme Oxygenase-1 to Improve Mitochondrial Function

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Cited by 7 publications
(3 citation statements)
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“…Interestingly, HO-1 knockout increases ROS and MDA levels and decreases SOD and ATP levels. HO-1 deficiency aggravates mitochondrial swelling, crest relaxation, and vacuole degeneration, indicating the key role of HO-1 in maintaining mitochondrial energy production and resisting oxidative damage in the hippocampus (73). In an SAE rat model, Li et al found that EA DU20, ST36, and LI11 acupoints upregulated the expression of Nrf-2 mRNA and HO-1 protein, increased the SOD level, reduced the MDA level in the hippocampus, reduced the loss of neurons in the hippocampal CA1 area, and increased the 14-day survival rate (75).…”
Section: Brainmentioning
confidence: 99%
See 1 more Smart Citation
“…Interestingly, HO-1 knockout increases ROS and MDA levels and decreases SOD and ATP levels. HO-1 deficiency aggravates mitochondrial swelling, crest relaxation, and vacuole degeneration, indicating the key role of HO-1 in maintaining mitochondrial energy production and resisting oxidative damage in the hippocampus (73). In an SAE rat model, Li et al found that EA DU20, ST36, and LI11 acupoints upregulated the expression of Nrf-2 mRNA and HO-1 protein, increased the SOD level, reduced the MDA level in the hippocampus, reduced the loss of neurons in the hippocampal CA1 area, and increased the 14-day survival rate (75).…”
Section: Brainmentioning
confidence: 99%
“…Interestingly, HO-1 knockout increases ROS and MDA levels and decreases SOD and ATP levels. HO-1 deficiency aggravates mitochondrial swelling, crest relaxation, and vacuole degeneration, indicating the key role of HO-1 in maintaining mitochondrial energy production and resisting oxidative damage in the hippocampus ( 73 ). In an SAE rat model, Li et al.…”
Section: Acupuncture Prevents Sepsis Organ Dysfunction By Inhibiting ...mentioning
confidence: 99%
“…In addition, Mu et al [119] first demonstrated that EA at “Zusanli (ST36)” and “Baihui (GV20)” improved LPS-induced hippocampal injury by improving mitochondrial function and that EA treatment reduced neuronal damage in LPS-exposed mice while improving mitochondrial respiratory function, energy metabolism, and mitochondrial morphology. It was also discovered that HO-1 knockdown exacerbated LPS-induced hippocampal injury, decreased mitochondrial respiratory function, increased mitochondrial swelling, cristae relaxation, and vacuolar degeneration and that EA did not reverse the hippocampal injury and mitochondrial dysfunction caused by LPS after HO-1 knockdown.…”
Section: Immunological Basis Of Ea To Alleviate Sepsismentioning
confidence: 99%