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Downregulation of nitric oxide by electroacupuncture against hypoxic‑ischemic brain damage in rats via nuclear factor‑κB/neuronal nitric oxide synthase.

Liu Y, Li W, Hu L, Liu Y, Li B, Sun C, Zhang C, Zou L - Mol Med Rep (2014)

Bottom Line: In addition, treatment with EA significantly downregulated the expression of nNOS and NF‑κB in the rat cortex cells (*P<0.05, **P<0.01, compared with the control groups).The results also indicated that treatment with EA downregulated the NO content of cortical cells against HIBD via the NF‑κB/nNOS pathway and further implied that the hydrogen sulfide/CBS system may be involved in the process.The present study provided a significant reference for the prevention and treatment of HIBD using the EA technique and also described a novel protective mechanism.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing 100853, P.R. China.

ABSTRACT
The present study aimed to investigate the role of nitric oxide (NO) against perinatal hypoxic‑ischemic brain damage (HIBD) in rats by electroacupuncture (EA) and to examine its potential neuroprotective mechanism. NO content, the number of positive cells, neuronal nitric oxide synthase (nNOS) and nuclear factor‑κB (NF‑κB) in rat cortex cells were determined. The results demonstrated that treatment with EA significantly downregulated the NO content in the cortex cells (*P<0.05, **P<0.01, compared with the control groups) and alleviated cell damage in the cortex of rats with HIBD. The activator, S‑adenosyl‑L‑methionine and the inhibitor, hydroxylamine of cystathionine‑β‑synthase (CBS), aggravated and remitted the hypoxic damage in the cortex cells, respectively. In addition, treatment with EA significantly downregulated the expression of nNOS and NF‑κB in the rat cortex cells (*P<0.05, **P<0.01, compared with the control groups). The results also indicated that treatment with EA downregulated the NO content of cortical cells against HIBD via the NF‑κB/nNOS pathway and further implied that the hydrogen sulfide/CBS system may be involved in the process. The present study provided a significant reference for the prevention and treatment of HIBD using the EA technique and also described a novel protective mechanism.

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Related in: MedlinePlus

Column chart analysis of the NO content in cortex cells. The chart indicates that EA downregulates the NO content in the cortex cells, with a significant difference compared with each control (*P<0.05, **P<0.01). NO, nitric oxide; EA, electroaccupuncture; HIBD, hypoxic-ischemia brain damage; SAM, S-adenosyl-L-methionine; HA, hydroxylamine.
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f1-mmr-11-02-0837: Column chart analysis of the NO content in cortex cells. The chart indicates that EA downregulates the NO content in the cortex cells, with a significant difference compared with each control (*P<0.05, **P<0.01). NO, nitric oxide; EA, electroaccupuncture; HIBD, hypoxic-ischemia brain damage; SAM, S-adenosyl-L-methionine; HA, hydroxylamine.

Mentions: The NO content in the cortex of the Sham, Sham + EA, HIBD, HIBD + EA, HIBD + SAM, HIBD + SAM + EA, HIBD + HA and HIBD + HA + EA groups was 2.3614±0.3807, 1.4165±0.2592, 3.5269±1.6970, 1.6787±0.7213, 5.5101±2.5914, 2.6041±0.7773, 2.8041±0.8377 and 1.6784±0.7917, respectively (Table I). HIBD significantly upregulated the NO content in the cortex cells compared with the Sham group. In addition, treatment with SAM further upregulated the NO content of the cortex cells in the HIBD rats compared with the Sham group. However, treatment with HA downregulated the NO content of the cortex cells compared with the Sham group. Furthermore, EA treatment downregulated the NO content in the Sham + EA, HIBD + EA, HIBD + SAM + EA and HIBD + HA + EA groups compared with those of the control groups, including Sham (*P<0.05), HIBD (**P<0.01), HIBD + SAM (**P<0.01) and HIBD + HA (*P<0.05), particularly in the HIBD and HIBD + SAM groups (Fig. 1).


Downregulation of nitric oxide by electroacupuncture against hypoxic‑ischemic brain damage in rats via nuclear factor‑κB/neuronal nitric oxide synthase.

Liu Y, Li W, Hu L, Liu Y, Li B, Sun C, Zhang C, Zou L - Mol Med Rep (2014)

Column chart analysis of the NO content in cortex cells. The chart indicates that EA downregulates the NO content in the cortex cells, with a significant difference compared with each control (*P<0.05, **P<0.01). NO, nitric oxide; EA, electroaccupuncture; HIBD, hypoxic-ischemia brain damage; SAM, S-adenosyl-L-methionine; HA, hydroxylamine.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4262503&req=5

f1-mmr-11-02-0837: Column chart analysis of the NO content in cortex cells. The chart indicates that EA downregulates the NO content in the cortex cells, with a significant difference compared with each control (*P<0.05, **P<0.01). NO, nitric oxide; EA, electroaccupuncture; HIBD, hypoxic-ischemia brain damage; SAM, S-adenosyl-L-methionine; HA, hydroxylamine.
Mentions: The NO content in the cortex of the Sham, Sham + EA, HIBD, HIBD + EA, HIBD + SAM, HIBD + SAM + EA, HIBD + HA and HIBD + HA + EA groups was 2.3614±0.3807, 1.4165±0.2592, 3.5269±1.6970, 1.6787±0.7213, 5.5101±2.5914, 2.6041±0.7773, 2.8041±0.8377 and 1.6784±0.7917, respectively (Table I). HIBD significantly upregulated the NO content in the cortex cells compared with the Sham group. In addition, treatment with SAM further upregulated the NO content of the cortex cells in the HIBD rats compared with the Sham group. However, treatment with HA downregulated the NO content of the cortex cells compared with the Sham group. Furthermore, EA treatment downregulated the NO content in the Sham + EA, HIBD + EA, HIBD + SAM + EA and HIBD + HA + EA groups compared with those of the control groups, including Sham (*P<0.05), HIBD (**P<0.01), HIBD + SAM (**P<0.01) and HIBD + HA (*P<0.05), particularly in the HIBD and HIBD + SAM groups (Fig. 1).

Bottom Line: In addition, treatment with EA significantly downregulated the expression of nNOS and NF‑κB in the rat cortex cells (*P<0.05, **P<0.01, compared with the control groups).The results also indicated that treatment with EA downregulated the NO content of cortical cells against HIBD via the NF‑κB/nNOS pathway and further implied that the hydrogen sulfide/CBS system may be involved in the process.The present study provided a significant reference for the prevention and treatment of HIBD using the EA technique and also described a novel protective mechanism.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing 100853, P.R. China.

ABSTRACT
The present study aimed to investigate the role of nitric oxide (NO) against perinatal hypoxic‑ischemic brain damage (HIBD) in rats by electroacupuncture (EA) and to examine its potential neuroprotective mechanism. NO content, the number of positive cells, neuronal nitric oxide synthase (nNOS) and nuclear factor‑κB (NF‑κB) in rat cortex cells were determined. The results demonstrated that treatment with EA significantly downregulated the NO content in the cortex cells (*P<0.05, **P<0.01, compared with the control groups) and alleviated cell damage in the cortex of rats with HIBD. The activator, S‑adenosyl‑L‑methionine and the inhibitor, hydroxylamine of cystathionine‑β‑synthase (CBS), aggravated and remitted the hypoxic damage in the cortex cells, respectively. In addition, treatment with EA significantly downregulated the expression of nNOS and NF‑κB in the rat cortex cells (*P<0.05, **P<0.01, compared with the control groups). The results also indicated that treatment with EA downregulated the NO content of cortical cells against HIBD via the NF‑κB/nNOS pathway and further implied that the hydrogen sulfide/CBS system may be involved in the process. The present study provided a significant reference for the prevention and treatment of HIBD using the EA technique and also described a novel protective mechanism.

Show MeSH
Related in: MedlinePlus