Neuroprotective effects of Buyang Huanwu decoction against hydrogen peroxide induced oxidative injury in Schwann cells

Yang, Shuai; Gao, Qing; Shen, Xing; Feng, Xiaowen; Peng, Lei; Dong, Hongbo; Liu, Bao; Zhang, Jing; Hu, Yaomin; Li, Guibao; Song, Tao; Li, Zhenhua; Sun, Jinhao

doi:10.1016/j.jep.2011.07.014

Cited by 32 publications

(28 citation statements)

References 27 publications

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“…In addition, oxidative stress might play a critical role in reduction of NCV and alteration in myelin structural integrity (Hamilton et al, 2013). Schwann cells are important in nerve regeneration (Yang et al, 2011). Our previous experiment showed that TLN could ameliorate sciatic nerve injuries through activating Nrg1/ErbB2→Erk/Bad Schwann cell survival signaling pathway .…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Tang Luo Ning effect on attenuating of oxidative stress in sciatic nerve of STZ-induced diabetic rats

Yang

Yao

et al. 2015

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 99%

Mechanism of Tang Luo Ning effect on attenuating of oxidative stress in sciatic nerve of STZ-induced diabetic rats

Yang

Yao

et al. 2015

Journal of Ethnopharmacology

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“…BYHWD also enhances the activity of superoxide dismutase (SOD) in rats with myocardial ischemia [54]. In vitro , BYHWD protects Schwann cells from hydrogen peroxide (H2O2) damage [55]. BYHWD also decreases H 2 O 2 -induced apoptosis in human umbilical vein endothelial cells (HUVECs) [56].…”

Section: Discussionmentioning

confidence: 99%

An Intersectional Study of LncRNAs and mRNAs Reveals the Potential Therapeutic Targets of Buyang Huanwu Decoction in Experimental Intracerebral Hemorrhage

Cui

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Both experimental and clinical studies have revealed satisfactory effects of the traditional Chinese formula Buyang Huanwu decoction (BYHWD) in improving post-intracerebral hemorrhage (ICH) neurological deficiencies. However, the multifaceted mechanisms of BYHWD in ICH treatment are not comprehensively understood. The present study explored various therapeutic targets of BYHWD by using lncRNA and mRNA transcriptomics. Methods: LncRNA and mRNA microarrays were used to identify differentially expressed genes. ICH-induced upregulated genes (ICH vs sham) and BYHWD-induced downregulated genes (BYHWD vs ICH) were first identified. The intersection between these 2 sets was determined to identify ICH-induced highly expressed genes that were reversed by BYHWD. Then, the genes downregulated after ICH and the genes upregulated after BYHWD treatment were used to generate another set of intersections. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were subsequently performed to determine relative biological functions and signaling transduction pathways according to genes within the intersections. Quantitative real-time PCR was used to validate changes in gene expression observed using the microarray. Finally, a lncRNA-mRNA co-expression network was established to identify links among the genes within the intersections. Results: A total of 18 differentially expressed lncRNAs and 33 differentially expressed mRNAs were identified using 2 lncRNA arrays (ICH vs sham and BYHWD vs ICH). The altered genes were enriched in the hemoglobin complex, oxygen transport and oxygen transporter and were closely associated with pyruvate metabolism. The co-expression network consisted of 53 nodes and 595 connections (308 positive interactions and 287 negative interactions). Conclusion: The hemoglobin complex, oxygen transport, oxygen transporter activity and pyruvate metabolism are possible therapeutic targets of BYHWD in ICH treatment. The present study provides the basis and direction for future investigations to explore the mechanisms by which BYHWD protects against long-term neurological deficiencies after ICH.

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“…Systematic reviews and meta-analyses of BYHWD have demonstrated that BYHWD is generally safe and possesses substantial neuroprotective action in patients and various animal models of focal ischemia (2,3). The protective effect of BYHWD against focal ischemia involves multiple mechanisms, for instance, reducing calcium overload injury, attenuating reactive oxygen stress (ROS) (4), inhibiting the inflammatory response and apoptosis (5), and promoting nerve regeneration and synapse formation (6).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of glutamate metabolism by BYHWD in cultured astrocytes following oxygen-glucose deprivation/reoxygenation in part depends on the activation of p38 MAPK

Guan

Zhou

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Recent studies have demonstrated that Buyang Huanwu Decoction (BYHWD) decreased glutamate levels subsequent to cerebral ischemia. Glutamate transporter-1 (GLT-1) and glutamine synthetase (GS), which are located in astrocytes, mainly contribute to glutamate transportation, thus reducing glutamate concentration. BYHWD has previously been demonstrated to upregulate GLT-1 and GS following ischemia in vivo. However, whether BYHWD can directly influence astrocytic GLT-1/GS levels remains unknown. In the present study, the effect of BYHWD containing serum (BYHWD-CS) on GLT-1/GS levels in astrocytes following oxygen-glucose deprivation/reoxygenation (OGD/R) was investigated. The results revealed that BYHWD-CS enhanced the expression levels of GLT-1 and GS in cultured astrocytes, which reduced glutamate concentration in the culture medium. Meanwhile, increased p38 mitogen-activated protein kinase (p38 MAPK) was phosphorylated (activation form) by BYHWD-CS in cultured astrocytes, and the specific p38 inhibitor SB203580 blocked the increase of GLT-1/GS accompanied by decreased cell viability. Furthermore, SB203580 suppressed the effect of BYHWD-CS on the level of glial fibrillary acidic protein (an astrocytic marker), thus confirming that astrocytes are directly involved in the protective role of BYHWD after OGD/R. These findings suggest that BYHWD upregulates GLT-1 and GS via p38 MAPK activation, and protects cultured astrocytes from death caused by OGD/R (typical in vitro model), which complemented the role of astrocytes in the protective effect of BYHWD.

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Neuroprotective effects of Buyang Huanwu decoction against hydrogen peroxide induced oxidative injury in Schwann cells

Cited by 32 publications

References 27 publications

Mechanism of Tang Luo Ning effect on attenuating of oxidative stress in sciatic nerve of STZ-induced diabetic rats

Mechanism of Tang Luo Ning effect on attenuating of oxidative stress in sciatic nerve of STZ-induced diabetic rats

An Intersectional Study of LncRNAs and mRNAs Reveals the Potential Therapeutic Targets of Buyang Huanwu Decoction in Experimental Intracerebral Hemorrhage

Upregulation of glutamate metabolism by BYHWD in cultured astrocytes following oxygen-glucose deprivation/reoxygenation in part depends on the activation of p38 MAPK

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