scholarly journals Hydrogen Peroxide and Nitric Oxide are Involved in Salicylic Acid-Induced Salvianolic Acid B Production in Salvia miltiorrhiza Cell Cultures

Molecules ◽  
2014 ◽  
Vol 19 (5) ◽  
pp. 5913-5924 ◽  
Author(s):  
Hongbo Guo ◽  
Xiaolin Dang ◽  
Juane Dong
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Salicylic Acid ◽  
Cell Cultures ◽  
Salvia Miltiorrhiza ◽  
Salvianolic Acid B ◽  
Salvianolic Acid

scholarly journals Evaluation of antigenotoxic potential of salvianolic acid B with hydrogen peroxide on human peripheral blood leukocytes in vitro

2017 ◽  
Vol 51 (2) ◽  
pp. 39-45
Author(s):  
Milena Jankovic ◽  
Lada Zivkovic ◽  
Andrea Pirkovic ◽  
Dijana Topalovic ◽  
Dragana Dekanski ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Peripheral Blood ◽  
Human Peripheral Blood ◽  
Salvianolic Acid B ◽  
Peripheral Blood Leukocytes ◽  
Blood Leukocytes ◽  
Salvianolic Acid

scholarly journals Salvianolic Acid B Improves Postresuscitation Myocardial and Cerebral Outcomes in a Murine Model of Cardiac Arrest: Involvement of Nrf2 Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Qing-Qi Ji ◽  
Yan-Jie Li ◽  
Ying-Hua Wang ◽  
Zi Wang ◽  
Liang Fang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Signaling Pathway ◽  
Murine Model ◽  
Nuclear Translocation ◽  
Salvia Miltiorrhiza ◽  
Left Ventricular ◽  
Salvianolic Acid B ◽  
Mitochondrial Morphology ◽  
Salvianolic Acid ◽  
Nrf2 Signaling Pathway

Survival and outcome of cardiac arrest (CA) are dismal despite improvements in cardiopulmonary resuscitation (CPR). Salvianolic acid B (Sal B), extracted from Salvia miltiorrhiza, has been investigated for its cardioprotective properties in cardiac remodeling and ischemic heart disease, but less is known about its role in CA. The aim of this study was to learn whether Sal B improves cardiac and neurologic outcomes after CA/CPR in mice. Female C57BL/6 mice were subjected to eight minutes of CA induced by an intravenous injection of potassium chloride (KCl), followed by CPR. After 30 seconds of CPR, mice were blindly randomized to receive either Sal B (20 mg/kg) or vehicle (normal saline) intravenously. Hemodynamic variables and indices of left ventricular function were determined before CA and within three hours after CPR, the early postresuscitation period. Sal B administration resulted in a remarkable decrease in the time required for the return of spontaneous circulation (ROSC) in animals that successfully resuscitated compared to the vehicle-treated mice. Myocardial performance, including cardiac output and left ventricular systolic (dp/dtmax) and diastolic (dp/dtmin) function, was clearly ameliorated within three hours of ROSC in the Sal B-treated mice. Moreover, Sal B inhibited CA/CPR-induced cardiomyocyte apoptosis and preserved mitochondrial morphology and function. Mechanistically, Sal B dramatically promoted Nrf2 nuclear translocation through the downregulation of Keap1, which resulted in the expression of antioxidant enzymes, including HO-1 and NQO1, thereby counteracted the oxidative damage in response to CA/CPR. The aforementioned antiapoptotic and antioxidant effects of Sal B were impaired in the setting of gene silencing of Nrf2 with siRNA in vitro model. These improvements were associated with better neurological function and increased survival rate (75% vs. 40%, p<0.05) up to 72 hours postresuscitation. Our findings suggest that the administration of Sal B improved cardiac function and neurological outcomes in a murine model of CA via activating the Nrf2 antioxidant signaling pathway, which may represent a novel therapeutic strategy for the treatment of CA.

scholarly journals Protective Effects of Active Compounds from Salviae miltiorrhizae Radix against Glutamate-Induced HT-22 Hippocampal Neuronal Cell Death

Processes ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 914
Author(s):  
Hung Manh Phung ◽  
Sullim Lee ◽  
Ki Sung Kang
Keyword(s):  
Cell Death ◽  
Rosmarinic Acid ◽  
Calcium Influx ◽  
Salvia Miltiorrhiza ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Salvianolic Acid B ◽  
Tanshinone Iia ◽  
Salvianolic Acid

Oxidative stress is considered one of the factors that cause dysfunction and damage of neurons, causing diseases such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD).Recently, natural antioxidant sources have emerged as one of the main research areas for the discovery of potential neuroprotectants that can be used to treat neurological diseases. In this research, we assessed the neuroprotective effect of a 70% ethanol Salvia miltiorrhiza Radix (SMR) extract and five of its constituent compounds (tanshinone IIA, caffeic acid, salvianolic acid B, rosmarinic acid, and salvianic acid A) in HT-22 hippocampal cells. The experimental data showed that most samples were effective in attenuating the cytotoxicity caused by glutamate in HT-22 cells, except for rosmarinic acid and salvianolic acid B. Of the compounds tested, tanshinone IIA (TS-IIA) exerted the strongest effect in protecting HT-22 cells against glutamate neurotoxin. Treatment with 400 nM TS-IIA restored HT-22 cell viability almost completely. TS-IIA prevented glutamate-induced oxytosis by abating the accumulation of calcium influx, reactive oxygen species, and phosphorylation of mitogen-activated protein kinases. Moreover, TS-IIA inhibited glutamate-induced cytotoxicity by reducing the activation and phosphorylation of p53, as well as by stimulating Akt expression. This research suggested that TS-IIA is a potential neuroprotective component of SMR, with the ability to protect against neuronal cell death induced by excessive amounts of glutamate.

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