Salvianolic acid B attenuates apoptosis and inflammation via SIRT1 activation in experimental stroke rats

Lv, Hongdi; Wang, Ling; Shen, Jinchang; Hao, Shaojun; Aimin, Ming; Xi-dong, Wang; Su, Feng; Zhang, Zhengchen

doi:10.1016/j.brainresbull.2015.05.002

Cited by 110 publications

(79 citation statements)

References 33 publications

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“…In addition, numerous studies have reported that SalB is neuroprotective in various central nervous system diseases [8,12,15]. However, to our knowledge, no study has yet investigated the potential benefits in experimental SAH.…”

Section: Discussionmentioning

confidence: 99%

“…Multiple studies have shown that SalB possesses antioxidative and neuroprotective activities in vivo and in vitro [8–11]. For instance, recent research showed that SalB effectively attenuates oxidative stress-related disorders, such as myocardial ischemia and reperfusion, cerebral ischemia, and diabetes [12–14]. In addition, SalB can easily pass the blood-brain barrier and act directly on the central nervous system.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, SalB can easily pass the blood-brain barrier and act directly on the central nervous system. Studies have shown that SalB has neuroprotective activity in traumatic brain injury, stroke, Alzheimer’s disease, and Parkinson’s disease [12,15–17]. However, no study has investigated whether SalB is beneficial in experimental SAH.…”

Section: Introductionmentioning

confidence: 99%

“…Intriguingly, SalB was shown to induce activation of the Nrf2 signaling pathway in a variety of disease models [15,26,27]. Additionally, SalB is a potent activator of sirtuin 1 (SIRT1) [12,28,29], a nicotinamide adenine dinucleotide-dependent deacetylase implicated in a wide range of cellular functions. Mounting evidence indicates that SIRT1 activation ameliorates brain injury after SAH and plays a key role in regulating the Nrf2 signaling pathway [2,30–32].…”

Section: Introductionmentioning

confidence: 99%

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Cerebroprotection by salvianolic acid B after experimental subarachnoid hemorrhage occurs via Nrf2- and SIRT1-dependent pathways

Zhang

et al. 2018

Free Radical Biology and Medicine

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Salvianolic acid B (SalB), a natural polyphenolic compound extracted from the herb of Salvia miltiorrhiza, possesses antioxidant and neuroprotective properties and has been shown to be beneficial for diseases that affect vasculature and cognitive function. Here we investigated the protective effects of SalB against subarachnoid hemorrhage (SAH)-induced oxidative damage, and the involvement of underlying molecular mechanisms. In a rat model of SAH, SalB inhibited SAH-induced oxidative damage. The reduction in oxidative damage was associated with suppressed reactive oxygen species generation; decreased lipid peroxidation; and increased glutathione peroxidase, glutathione, and superoxide dismutase activities. Concomitant with the suppressed oxidative stress, SalB significantly reduced neurologic impairment, brain edema, and neural cell apoptosis after SAH. Moreover, SalB dramatically induced nuclear factor-erythroid 2-related factor 2 (Nrf2) nuclear translocation and increased expression of heme oxygenase-1 and NADPH: quinine oxidoreductase-1. In a mouse model of SAH, Nrf2 knockout significantly reversed the antioxidant effects of SalB against SAH. Additionally, SalB activated sirtuin 1 (SIRT1) expression, whereas SIRT1-specific inhibitor sirtinol pretreatment significantly suppressed SalB-induced SIRT1 activation and Nrf2 expression. Sirtinol pretreatment also reversed the antioxidant and neuroprotective effects of SalB. In primary cultured cortical neurons, SalB suppressed oxidative damage, alleviated neuronal degeneration, and improved cell viability. These beneficial effects were associated with activation of the SIRT1 and Nrf2 signaling pathway and were reversed by sirtinol treatment. Taken together, these in vivo and in vitro findings suggest that SalB provides protection against SAH-triggered oxidative damage by upregulating the Nrf2 antioxidant signaling pathway, which may be modulated by SIRT1 activation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cerebroprotection by salvianolic acid B after experimental subarachnoid hemorrhage occurs via Nrf2- and SIRT1-dependent pathways

Zhang

et al. 2018

Free Radical Biology and Medicine

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“…Although its most common use is in the treatment of cardio-cerebral vascular diseases [14][15][16], Sal B is recently reported to possess a number of potential implications in the treatment of insulin resistance, obesity, and type 2 diabetes [17][18][19][20]. Sal B or Salvia miltiorrhiza extract improved glycemic control, dyslipidemia, and insulin sensitivity in high fat diet and streptozocin-induced type 2 diabetic rats [17,19].…”

Section: Introductionmentioning

confidence: 99%

Salvianolic Acid B Ameliorates Hyperglycemia and Dyslipidemia in db/db Mice through the AMPK Pathway

Huang

Zhou

Zhang

et al. 2016

Cell Physiol Biochem

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Background/Aims: Salvianolic acid B (Sal B), a major polyphenolic compound of Salvia miltiorrhiza Bunge, has been shown to possess potential antidiabetic activities. However, the action mechanism of SalB in type 2 diabetes has not been investigated extensively. The present study was designed to investigate the effects of Sal B on diabetes-related metabolic changes in a spontaneous model of type 2 diabetes, as well as its potential molecular mechanism. Methods: Male C57BL/KsJ-db/db mice were orally treated with Sal B (50 and 100 mg/kg) or metformin (positive drug, 300 mg/kg) for 6 weeks. Results: Both doses of Sal B significantly decreased fasting blood glucose, serum insulin, triglyceride and free fatty acid levels, reduced hepatic gluconeogenic gene expression and improved insulin intolerance in db/db mice. High dose Sal B also significantly improved glucose intolerance, increased hepatic glycolytic gene expression and muscle glycogen content, and ameliorated histopathological alterations of pancreas, similar to metformin. Sal B treatment resulted in increased phosphorylated AMP-activated protein kinase (p-AMPK) protein expression in skeletal muscle and liver, increased glucose transporter 4 (GLUT4) and glycogen synthase protein expressions in skeletal muscle, and increased peroxisome proliferator-activated receptor alpha (PPARα) and phosphorylated acetyl CoA carboxylase (p-ACC) protein expressions in liver. Conclusion: Our data suggest that Sal B displays beneficial effects in the prevention and treatment of type 2 diabetes at least in part via modulation of the AMPK pathway.

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Hypoxic conditioned medium derived from bone marrow mesenchymal stromal cells protects against ischemic stroke in rats

Jiang

et al. 2018

Journal Cellular Physiology

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In recent years, studies have shown that the secretome of bone marrow mesenchymal stromal cells (BMSCs) contains many growth factors, cytokines, and antioxidants, which may provide novel approaches to treat ischemic diseases. Furthermore, the secretome may be modulated by hypoxic preconditioning. We hypothesized that conditioned medium (CM) derived from BMSCs plays a crucial role in reducing tissue damage and improving neurological recovery after ischemic stroke and that hypoxic preconditioning of BMSCs robustly improves these activities. Rats were subjected to ischemic stroke by middle cerebral artery occlusion and then intravenously administered hypoxic CM, normoxic CM, or Dulbecco modified Eagle medium (DMEM, control). Cytokine antibody arrays and label-free quantitative proteomics analysis were used to compare the differences between hypoxic CM and normoxic CM. Injection of normoxic CM significantly reduced the infarct area and improved neurological recovery after stroke compared with administering DMEM. These outcomes may be associated with the attenuation of apoptosis and promotion of angiogenesis. Hypoxic preconditioning significantly enhanced these therapeutic effects. Fourteen proteins were significantly increased in hypoxic CM compared with normoxic CM as measured by cytokine arrays. The label-free quantitative proteomics analysis revealed 163 proteins that were differentially expressed between the two groups, including 107 upregulated proteins and 56 downregulated proteins. Collectively, our results demonstrate that hypoxic CM protected brain tissue from ischemic injury and promoted functional recovery after stroke in rats and that hypoxic CM may be the basis of a potential therapy for stroke patients.

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Salvianolic acid B attenuates apoptosis and inflammation via SIRT1 activation in experimental stroke rats

Cited by 110 publications

References 33 publications

Cerebroprotection by salvianolic acid B after experimental subarachnoid hemorrhage occurs via Nrf2- and SIRT1-dependent pathways

Cerebroprotection by salvianolic acid B after experimental subarachnoid hemorrhage occurs via Nrf2- and SIRT1-dependent pathways

Salvianolic Acid B Ameliorates Hyperglycemia and Dyslipidemia in db/db Mice through the AMPK Pathway

Hypoxic conditioned medium derived from bone marrow mesenchymal stromal cells protects against ischemic stroke in rats

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