Limits...
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.

Show MeSH

Related in: MedlinePlus

Assay of the expression level of NF-κB in the cortex by IHC and column chart analysis. (A) IHC assay of the expression of NF-κB in the cortex. (B) Column chart analysis of the expression of NF-κB in the cortex. The results indicated that EA downregulates the expression of NF-κB in the cortex, with a significant difference compared with each control (*P<0.05, **P<0.01). IHC, immunohistochemistry; NF-κB, nuclear factor-κB; EA, electroacupuncture; HIBD, hypoxic-ischemia brain damage; SAM, S-adenosyl-L-methionine; HA, hydroxylamine.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4262503&req=5

f4-mmr-11-02-0837: Assay of the expression level of NF-κB in the cortex by IHC and column chart analysis. (A) IHC assay of the expression of NF-κB in the cortex. (B) Column chart analysis of the expression of NF-κB in the cortex. The results indicated that EA downregulates the expression of NF-κB in the cortex, with a significant difference compared with each control (*P<0.05, **P<0.01). IHC, immunohistochemistry; NF-κB, nuclear factor-κB; EA, electroacupuncture; HIBD, hypoxic-ischemia brain damage; SAM, S-adenosyl-L-methionine; HA, hydroxylamine.

Mentions: HIBD upregulated the expression of NF-κB in the cortex cells compared with the Sham group and treatment with SAM significantly upregulated the expression of NF-κB in the cortex cells of HIBD rats compared with Sham treatment. However, treatment with HA downregulated the expression of NF-κB in the cortex cells of HIBD rats compared with the Sham group and treatment with EA downregulated the expression of NF-κB in the cortex cells compared with the control groups (Fig. 4A). A significant difference in the expression of NF-κB was observed between the Sham + EA and the Sham groups (Fig. 4B; **P<0.05). Similarly, a significant difference was identified in the expression of NF-κB between the other EA groups and the control groups, including HIBD (Fig. 4B; **P<0.01), HIBD + SAM (Fig. 4B; *P<0.05) and HIBD + HA (Fig. 4B; **P<0.01).


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)

Assay of the expression level of NF-κB in the cortex by IHC and column chart analysis. (A) IHC assay of the expression of NF-κB in the cortex. (B) Column chart analysis of the expression of NF-κB in the cortex. The results indicated that EA downregulates the expression of NF-κB in the cortex, with a significant difference compared with each control (*P<0.05, **P<0.01). IHC, immunohistochemistry; NF-κB, nuclear factor-κB; EA, electroacupuncture; 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

f4-mmr-11-02-0837: Assay of the expression level of NF-κB in the cortex by IHC and column chart analysis. (A) IHC assay of the expression of NF-κB in the cortex. (B) Column chart analysis of the expression of NF-κB in the cortex. The results indicated that EA downregulates the expression of NF-κB in the cortex, with a significant difference compared with each control (*P<0.05, **P<0.01). IHC, immunohistochemistry; NF-κB, nuclear factor-κB; EA, electroacupuncture; HIBD, hypoxic-ischemia brain damage; SAM, S-adenosyl-L-methionine; HA, hydroxylamine.
Mentions: HIBD upregulated the expression of NF-κB in the cortex cells compared with the Sham group and treatment with SAM significantly upregulated the expression of NF-κB in the cortex cells of HIBD rats compared with Sham treatment. However, treatment with HA downregulated the expression of NF-κB in the cortex cells of HIBD rats compared with the Sham group and treatment with EA downregulated the expression of NF-κB in the cortex cells compared with the control groups (Fig. 4A). A significant difference in the expression of NF-κB was observed between the Sham + EA and the Sham groups (Fig. 4B; **P<0.05). Similarly, a significant difference was identified in the expression of NF-κB between the other EA groups and the control groups, including HIBD (Fig. 4B; **P<0.01), HIBD + SAM (Fig. 4B; *P<0.05) and HIBD + HA (Fig. 4B; **P<0.01).

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