Neuron Regeneration and Proliferation Effects of Danshen and Tanshinone IIA

Shen, Jui-Lung; Chen, Yueh-Sheng; Lin, Jing‐Ying; Tien, Yun-Chen; Peng, Wen-Huang; Kuo, Chia‐Hua; Tzang, Bor‐Show; Wang, Hwai-Lee; Tsai, Fuu‐Jen; Chou, Ming-Chih; Huang, Chih‐Yang; Lin, Chien‐Chung

doi:10.1155/2011/378907

Cited by 27 publications

(17 citation statements)

References 34 publications

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“…In addition, elevating the proliferation ability of SCs is important for constructing tissue-engineered nerves (6). As a result, researchers have been exploring various promoting agents for SCs proliferation, such as interleukin-1β (14) and tanshinone IIA (15 Utilizing plant-derived traditional Chinese medicines to treat various types of diseases has a long history in East Asian countries, such as China, Korea and Japan (16). Furthermore, some western medicines are derived from major constituent of traditional Chinese medicine (17) Scutellaria baicalensis Georgi (Huangqin in Chinese), a traditional Chinese medicine, has been used to treat inflammation, fever, ulcers and cancer for hundreds of years (18)(19)(20) and a recent study has reported that flavonoids from the stems and leaves of S. baicalensis Georgi have neuroprotective effects (21).…”

Section: Introductionmentioning

confidence: 99%

Baicalin promotes the viability of Schwann cells in vitro by regulating neurotrophic factors

Zuo

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The proliferation and migration of Schwann cells (SCs) are key events in the process of peripheral nerve repair. This is required to promote the growth of SCs and is a challenge during the treatment of peripheral nerve injury. Baicalin is a natural herb-derived flavonoid compound, which has been reported to possess neuroprotective effects on rats with permanent brain ischemia and neuronal differentiation of neural stem cells. The association of baicalin with neuroprotection leads to the suggestion that baicalin may exert effects on the growth of SCs. In the present study, the effects of baicalin on SCs of RSC96 were investigated. RSC96 SCs were treated with various concentrations of baicalin (0, 5, 10 or 20 µM) for 2, 4 and 6 days. Cell attachment, viability and gene expression were monitored via the MTT assay and reverse transcription-quantitative polymerase chain reaction. The gene expression levels of several neurotrophic factors, such as glial cell-derived neurotrophic factor, brain-derived neurotrophic factor and ciliary neurotrophic factor, which are considered important factors in the process of never cell regeneration, were detected. The results indicated that baicalin was able to promote the viability of RSC96 SCs in a dose-dependent manner and the concentration of 20 µM of baicalin exhibited the greatest cell viability and gene expression of the studied neurotrophic factors. The present findings suggested that baicalin likely affects SCs metabolism, through modulating the expression of neurotrophic factors. To conclude, the present study indicates that baicalin may be potential therapeutic agent for treating peripheral nerve regeneration.

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Section: Introductionmentioning

confidence: 99%

Baicalin promotes the viability of Schwann cells in vitro by regulating neurotrophic factors

Zuo

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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“…Shen et al. (2011) reported that TSN IIA had a proliferative effect on neuronal cells; specifically, TSN IIA enhanced neuron regeneration [26]. Moreover, the neuroprotective effect of TSN IIA has also been reported in diabetic rats [27].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of tanshinone IIA against neuropathic pain in diabetic rats through the Nrf2/ARE and NF‐κB signaling pathways

Feng

Qiu

2018

The Kaohsiung J of Med Scie

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The study aims to investigate whether tanshinone (TSN) IIA affects diabetic neuropathic pain (DNP) via the Nrf2/AR and NF-κB signaling pathways. Rats were randomly assigned into DNP group, TSN group (injected with TSN IIA), TSN + DRB group (injected with TSN IIA and 15 mg/kg Nrf2/ARE inhibitors), TSN + PDTC group (injected with TSN IIA and 60 mg/kg NF-κB inhibitors) or control group. The first four groups were successfully established as DNP models after injection of streptozotocin. The blood glucose level, mechanical withdrawal threshold (MWT), thermal withdrawal latency (TWL), nerve conduction velocity (NCV) and antioxidase level were detected. Transmission electron microscopy and toluidine blue staining were utilized to observe the sciatic nerve. RT-qPCR and western blot were used to measure expression levels of Nrf2/ARE and NF-κB signaling pathway-related genes. Blood glucose, malondialdehyde (MDA) and erythrocyte glutathione peroxidase (GSH-Px) levels as well as expression of Keap1 and NF-κB were increased in the TSN, TSN + DRB and TSN + PDTC groups compared to control group. Furthermore, the MWT, TWL, NVC, and superoxide dismutase (SOD) levels and expression of Nrf2, heme oxygenase 1 (HO-1) and inhibitory kappa B (IκB) decreased in the treatment groups. The TSN + DRB and TSN + PDTC groups showed similar trend when compared with the TSN group, while the opposite trend was observed in the TSN group when compared with the DNP group. Our study demonstrates that TSN IIA alleviates neuropathic pain by activating the Nrf2/ARE signaling pathway and inhibiting the NF-κB signaling pathway in diabetic rats.

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“…Many flavonoids or phytoestrogens, such as Tanshinone IIA, protect the heart against hypertrophy via the estrogen receptor [22,23]. However, there is no direct evidence showing that estrogen has the same protective effect.…”

Section: Introductionmentioning

confidence: 99%

Treatment with 17β-Estradiol Reduced Body Weight and the Risk of Cardiovascular Disease in a High-Fat Diet-Induced Animal Model of Obesity

Wei

Huang

Jiang

et al. 2017

IJMS

Self Cite

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Estrogen receptor α (ERα) and estrogen receptor β (ERβ) play important roles in cardiovascular disease (CVD) prevention. Recently, these estrogen receptors were reconsidered as an important treatment target of obesity leading to CVD. In this study, 17β-estradiol (17β-E) replacement therapy applied to high-fat diet-induced obese C57B male mice and ovariectomized (OVX) rats were evaluated, and the protective effects against high-fat diet-induced obesity were assessed in C57B mouse hearts. The results showed that 17β-E treatment activated both ERα and ERβ, and ERβ levels increased in a dose-dependent manner in high-fat diet C57B mouse cardiomyocytes following 17β-E treatment. Notably, an almost 16% reduction in body weight was observed in the 17β-E-treated (12 µg/kg/day for 60 days) high-fat diet-induced obese C57B male mice. These results suggested that 17β-E supplements may reduce CVD risk due to obesity.

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Neuron Regeneration and Proliferation Effects of Danshen and Tanshinone IIA

Cited by 27 publications

References 34 publications

Baicalin promotes the viability of Schwann cells in vitro by regulating neurotrophic factors

Baicalin promotes the viability of Schwann cells in vitro by regulating neurotrophic factors

Neuroprotective effect of tanshinone IIA against neuropathic pain in diabetic rats through the Nrf2/ARE and NF‐κB signaling pathways

Treatment with 17β-Estradiol Reduced Body Weight and the Risk of Cardiovascular Disease in a High-Fat Diet-Induced Animal Model of Obesity

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