Tetramethylpyrazine Protects Against Oxygen-Glucose Deprivation-Induced Brain Microvascular Endothelial Cells Injury via Rho/Rho-kinase Signaling Pathway

Yang, Guang; Chen, Qian; Wang, Ning; Lin, Chia-Chen; Wang, Yan; Wang, Guangyun; Piao, Xinxin

doi:10.1007/s10571-016-0398-4

Cited by 40 publications

(26 citation statements)

References 59 publications

(66 reference statements)

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“…Tetramethylpyrazine (TMP), the main active component of Ligusticum wallichii Franchat , has been used extensively for the treatment of neurovascular diseases in China for centuries (6,7). As previously reported, TMP possesses therapeutic potential in a variety of diseases by mechanisms mediated by antioxidation and anti-apoptosis (8-10). Additionally, the neuroprotective effects of TMP in retinal diseases have been confirmed in vitro and in vivo (11,12).…”

Section: Introductionmentioning

confidence: 68%

“…Additionally, the neuroprotective effects of TMP in retinal diseases have been confirmed in vitro and in vivo (11,12). For example, Yang et al (10) revealed that TMP could preserve neuronal morphology and promote survival in retinal cell cultures, and protected cells against the cytotoxicity of high doses of hydrogen peroxide. Luo et al (13) suggested that TMP protects RGCs against N-methyl-D-aspartate-induced excitotoxicity.…”

Section: Introductionmentioning

confidence: 99%

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Tetramethylpyrazine protects retinal ganglion cells against H2O2‑induced damage via the�microRNA‑182/mitochondrial pathway

Wang

Ren

et al. 2019

Int J Mol Med

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Glaucoma is the leading cause of irreversible blindness worldwide; the apoptosis of the retinal ganglion cells (RGCs) is a hallmark of glaucoma. Tetramethylpyrazine (TMP) is the main active component of Ligusticum wallichii Franchat , and has been demonstrated to improve a variety of injuries through its antioxidative and antiapoptotic properties. However, these effects of TMP on glaucoma have not been studied. The present study aimed to investigate the potential role of TMP in glaucoma and to elucidate its possible mechanisms responsible for these effects. An in vitro model was generated, in which primary RGCs (PRGCs) were treated with H 2 O 2 . Our study revealed that TMP protected against H 2 O 2- induced injury to PRGCs, as evidenced by enhanced cell viability, reduced caspase 3 activity and decreased cell apoptosis. We also reported that TMP treatment inhibited reactive oxygen species (ROS) production and malondialdehyde levels, but upregulated the antioxidative enzyme superoxide dismutase. In particular, TMP significantly increased the expression of microRNA-182-5p (miR-182) in H 2 O 2 -treated PRGCs, which was selected as the target miRNA for further research. In addition, our findings suggested that the protective effects of TMP on H 2 O 2 -induced injury were attenuated by knockdown of miR-182. The results of a luciferase reporter assay demonstrated that Bcl-2 interacting protein 3 (BNIP3), an effector of mitochondria-mediated apoptosis, was a direct target of miR-182. In addition, TMP treatment significantly decreased the expression of BNIP3, Bax, cleaved-caspase-3 and cleaved-poly(ADP-ribose)polymerase, but increased that of Bcl-2. Also, TMP treatment decreased the release of cytochrome c from mitochondria and improved mitochondrial membrane potential in H 2 O 2 -treated RGCs. Of note, the inhibitory effects of TMP on the mitochondrial apoptotic pathway were suggested to be reversed by knockdown of miR-182. Collectively, our findings provide novel evidence that TMP protects PRGCs against H 2 O 2 -induced damage through suppressing apoptosis and oxidative stress via the miR-182/mitochondrial apoptotic pathway.

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Section: Introductionmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Tetramethylpyrazine protects retinal ganglion cells against H2O2‑induced damage via the�microRNA‑182/mitochondrial pathway

Wang

Ren

et al. 2019

Int J Mol Med

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“…Trans endothelial electrical resistance (TEER) was measured using an assembly containing current-passing and voltage measuring electrodes. Cell treating is the same as steps in detecting cell permeability24., 25.. MVECs were also seeded on top of transwell chamber in 24 wells (0.4-μm pore size).…”

Section: Methodsmentioning

confidence: 99%

Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury

Xing

et al. 2019

Acta Pharmaceutica Sinica B

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The loss of endothelial connective integrity and endothelial barrier dysfunction can lead to increased vascular injury, which is related to the activation of endothelial inflammasomes. There are evidences that low concentrations of aspirin can effectively prevent cardiovascular diseases. We hypothesized that low-dose aspirin could ameliorate endothelial injury by inhibiting the activation of NLRP3 inflammasomes and ultimately prevent cardiovascular diseases. Microvascular endothelial cells were stimulated by lipopolysaccharide (2 μg/mL) and administrated by 0.1–2 mmol/L aspirin. The wild type mice were stimulated with LPS (100 μg/kg/day), and 1 h later treated with aspirin (12.5, 62.5, or 125 mg/kg/day) and dexamethasone (0.0182 mg/kg/day) for 7 days. Plasma and heart were harvested for measurement of ELISA and immunofluorescence analyses. We found that aspirin could inhibit NLRP3 inflammasome formation and activation in vitro in dose-dependent manner and has correlation between the NLRP3 inflammasome and the ROS/TXNIP pathway. We also found that low-concentration aspirin could inhibit the formation and activation of NLRP3 inflammasome and restore the expression of the endothelial tight junction protein zonula occludens-1/2 (ZO1/2). We assume that aspirin can ameliorate the endothelial layer dysfunction by suppressing the activation of NLRP3 inflammasome.

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“…The possible mechanism of HBO induced downregulation of the Rho/ROCK pathway might be that increased oxygen content inhibited the activation of Rho and ROCK in intestinal tissue after HBO treatment. In addition, oxidative stress was probably involved in this process ( 31 , 32 ).…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Treatment Improves Intestinal Barrier Function After Spinal Cord Injury in Rats

et al. 2020

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Intestinal barrier dysfunction is often observed clinically after spinal cord injury (SCI) and seriously affects long-term quality of life. Hyperbaric oxygen (HBO) treatment has been proved to promote barrier function recovery after injury, but the influence of HBO on intestinal barrier function following SCI is unclear. We aimed to investigate the effect and mechanisms of HBO treatment on intestinal barrier function by measuring the level of tight junction (TJ) proteins and the Ras homolog (Rho)/Rho-associated coiled-coil forming protein kinase (ROCK) signaling pathway. SCI model was established in rats, and the animals were randomly assigned into three groups: sham-operation group (SH), SCI group and SCI+HBO group. In the SCI+HBO group, the rats inhaled 100% O 2 for 1 h at 2.0 atmospheres absolute pressure (ATA) once per day after surgery. Neurological function and intestinal permeability were assessed after surgery, and the jejunum tissue was excised for histological and intestinal barrier function evaluations. The protein levels of TJ and the Rho/ROCK signaling pathway were also measured. The results showed that in the SCI group, intestinal mucosal injury score, intestinal permeability, and levels of Rho and ROCK1 were higher, and TJ proteins occludin and ZO-1 were lower than those in the SH group (P < 0.01). HBO treatment significantly inhibited the expression of Rho and ROCK1, increased occludin and ZO-1 expression, decreased intestinal permeability, and alleviated intestinal mucosal injury as compared with the SCI group (P < 0.05, P < 0.01). The SCI+HBO group showed higher Basso-Beattie-Bresnahan (BBB) scores relative to the SCI group on postoperative days 7 and 14 (P < 0.01). There was a significant negative correlation between BBB score and intestinal mucosal injury score in rats after HBO treatment (P < 0.05). We concluded from this study that HBO treatment promoted the expression of TJ proteins possibly through inhibiting Rho/ROCK signaling pathway, which protected the intestinal barrier function and improved the intestinal permeability after SCI in rats.

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Tetramethylpyrazine Protects Against Oxygen-Glucose Deprivation-Induced Brain Microvascular Endothelial Cells Injury via Rho/Rho-kinase Signaling Pathway

Cited by 40 publications

References 59 publications

Tetramethylpyrazine protects retinal ganglion cells against H2O2‑induced damage via the�microRNA‑182/mitochondrial pathway

Tetramethylpyrazine protects retinal ganglion cells against H2O2‑induced damage via the�microRNA‑182/mitochondrial pathway

Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury

Hyperbaric Oxygen Treatment Improves Intestinal Barrier Function After Spinal Cord Injury in Rats

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