salvianolic acid a/inflammation

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Effect of salvianolic acid A and C compatibility on inflammatory cytokines in rats with unilateral ureteral obstruction.

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OBJECTIVE To investigate the effect of salvianolic acid A and C component molecules, which are involved in drug compatibility, on inflammatory cytokine expression that affects human chemokine ligand 5 (CCL5) and chemokine ligand 10 (CXCL10) levels in rats with unilateral ureteral obstruction

In silico analysis and experimental validation of molecular mechanisms of salvianolic acid A-inhibited LPS-stimulated inflammation, in RAW264.7 macrophages.

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OBJECTIVE The aim of this study was to explore mechanisms by which salvianolic acid A (SAA) revealed its anti-inflammatory activity, in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. METHODS Nitric oxide (NO) concentration was determined by the Griess reaction and cell viability was assessed by

Salvianolic acid A protects retinal pigment epithelium from OX-LDL-induced inflammation in an age-related macular degeneration model.

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Salvianolic acid A (Sal A), an active monomer of Salvia miltiorrhiza, is a phenolic carboxylic acid derivative. The present study was performed to investigate the underlying mechanism of the anti-inﬂammation effect of Sal A, especially focusing on mTOR-KEAP1-Nrf2 and P2X7R-PKR-NLRP3 signaling

Salvianolic acid A attenuated myocardial infarction-induced apoptosis and inflammation by activating Trx.

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Myocardial infarction (MI) is a leading cause of mortality worldwide and it is urgent to discover effective therapies. In this study, the protective effect of salvianolic acid A (SAL) on MI induced by left anterior descending coronary artery ligation surgery and H₂O₂-induced

Salvianolic acid A attenuates kidney injury and inflammation by inhibiting NF-κB and p38 MAPK signaling pathways in 5/6 nephrectomized rats.

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Salvianolic acid A (SAA) is a minor phenolic carboxylic acid extracted from Salviae miltiorrhizae Bunge (Danshen). SAA exhibits a variety of pharmacological activities, such as antioxidative, anti-thrombotic, neuroprotective, and anti-fibrotic effects, as well as protection from myocardial ischemia

Salvianolic acid A attenuates ischemia reperfusion induced rat brain damage by protecting the blood brain barrier through MMP-9 inhibition and anti-inflammation.

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Salvianolic acid A (SAA) is a water-soluble component from the root of Salvia Miltiorrhiza Bge, a traditional Chinese medicine, which has been used for the treatment of cerebrovascular diseases for centuries. The present study aimed to determine the brain protective effects of SAA against cerebral

Preventive effects of a natural anti-inflammatory agent Salvianolic acid A on acute kidney injury in mice.

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Acute kidney injury (AKI) is an abrupt loss of kidney function with high mortality. Inflammatory is considered driving the progression of AKI. Salvianolic acid A (SA), one of the major ingredients of Salvia miltiorrhiza Bunge, displays plenty of biological effects. Herein, the effect of SA on

Salvianolic acid A alleviates ischemic brain injury through the inhibition of inflammation and apoptosis and the promotion of neurogenesis in mice.

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Salvianolic acid A (SalA), a chemical type of caffeic acid trimer, has drawn great attention for its potent bioactivities against ischemia-induced injury both in vitro and in vivo. In this study, we evaluated SalA's protective effects against acute ischemic stroke by inducing middle cerebral artery

Salvianolic acid A protects against myocardial ischemia/reperfusion injury by reducing platelet activation and inflammation.

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The aim of the present study was to investigate the protective effect of salvianolic acid A (SAA) on myocardial ischemia/reperfusion injury in rats. SAA (10 mg/kg) or Tirofiban (60 µg/kg) was administered to rats by jugular vein injection 10 min before the initiation of reperfusion. After 3 h of

Salvianolic Acid A Exhibits Anti-Inflammatory and Antiarthritic Effects via Inhibiting NF-κB and p38/MAPK Pathways

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Introduction: Osteoarthritis (OA), a chronic joint disease, combines with massive inflammation and plays a vital role in cartilage degeneration. The main strategy in clinic is controlling inflammation, thereby treating osteoarthritis.

Salvianolic acid A attenuates cerebral ischemia/reperfusion injury induced rat brain damage, inflammation and apoptosis by regulating miR-499a/DDK1

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Background and objectives: Salvianolic acid A (SAA) is a main component derived from Salvia miltiorrhiza and has been revealed to protect against cerebral ischemia/reperfusion injury (CIRI). The present study was designed to evaluate the

Salvianolic acid A suppresses MMP-2 expression and restrains cancer cell invasion through ERK signaling in human nasopharyngeal carcinoma.

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Salvia miltiorrhiza Bunge, as known as Danshen, has used for the prevention and treatment of cardiovascular diseases clinically and anti-cancer activities. Salvianolic acid A (SAA), one of the most abundant ingredients, hydrophilic derivatives of Salvia miltiorrhiza Bunge, exerts a

Antimetastatic potentials of salvianolic acid A on oral squamous cell carcinoma by targeting MMP-2 and the c-Raf/MEK/ERK pathway.

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The metastasis of oral squamous cell carcinoma (OSCC) is one of the most important causes of cancer-related deaths. Thus, various therapeutic strategies have been developed to prevent the metastasis of OSCC. Salvianolic acid A (SAA), a traditional Chinese medicine, has antithrombosis, antiplatelet,

Salvianolic acid a attenuates limb ischemia/reperfusion injury in skeletal muscle of rats.

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Ischemia and reperfusion(I/R) injury can cause complications in applying blood flow treatment for atherosclerosis occlusion syndrome. Platelet activation and inflammatory reaction play a role in the procession of I/R injury. This study was designed to investigate the effects of Salvianolic Acid

Salvianolic acid A suppresses CCL-20 expression in TNF-α-treated macrophages and ApoE-deficient mice.

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OBJECTIVE The CC chemokine ligand-20 (CCL-20)/macrophage inflammatory protein-3α has been seen as one of the most important chemokines and played a key role in atherogenesis, but the mechanism that underlies the regulation of CCL-20 has not been established clearly yet. The aim of this study was to

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