Salvianolic acid B attenuates lipopolysaccharide-induced acute lung injury in rats through inhibition of apoptosis, oxidative stress and inflammation

Zhao, Dahai; Wu, Yujie; Liu, Shuting; Liu, Rong‐Yu

doi:10.3892/etm.2017.4534

Cited by 33 publications

(23 citation statements)

References 29 publications

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“…With the advantages of lower toxicity and higher safety, natural anti-oxidants have been diffusely utilized to protect cells resisting oxidative stress injury [24]. Sal-B is a hydrophilic caffeic acid derivative, which has been proven to exert antioxidative properties [25,26] [27].…”

Section: Discussionmentioning

confidence: 99%

Protective functions of salvianolic acid B in PC-12 cells against hydrogen peroxide-triggered damage by mediation of microRNA-26a

Liu

Fan

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Spinal cord injury (SCI) can lead to varying degrees of sensory and motor dysfunction. Salvianolic acid B (Sal-B) is the dominating bioactive constituent of Danshen, which has been reported to alleviate liver fibrosis and exert neuroprotective effects. But, the influence of Sal-B in SCI remains mysterious. The research planned to delve the protective function of Sal-B in hydrogen peroxide (H 2 O 2)-caused PC-12 cell injury. H 2 O 2-caused PC-12 cells injury model was built, CCK-8, Transwell and flow cytometry experiments were enforced to assess cell proliferation, migration and apoptosis. The microRNA (miR)-26a plasmid and the matching control were transfected into PC-12 cells, subsequently, the influence of miR-26a inhibition in H 2 O 2-corrupted PC-12 cells was evaluated. The cell growth-correlated factors and PI3K/AKT and MEK/ERK pathways were assayed through western blot assay. Results corroborated that Sal-B eased H 2 O 2-evoked injury in PC-12 cells. Ascended miR-26a was monitored in Sal-B and H 2 O 2exposed cells. MiR-26a inhibition annulled the protective action of Sal-B in H 2 O 2-corrupted cells. The protective function of Sal-B was enabled through activating PI3K/AKT and MEK/ERK pathways. These findings delineated that Sal-B protected PC-12 cells against H 2 O 2-caused injury through ascending miR-26a via initiating PI3K/AKT and MEK/ERK pathways. HIGHLIGHTS H 2 O 2 causes PC-12 cell injury; Sal-B eases H 2 O 2-caused PC-12 cell injury; Sal-B protects PC-12 cells against H 2 O 2-caused injury via elevating miR-26a; Sal-B activates AKT and MEK/ERK pathways via modulating miR-26a.

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Section: Discussionmentioning

confidence: 99%

Protective functions of salvianolic acid B in PC-12 cells against hydrogen peroxide-triggered damage by mediation of microRNA-26a

Liu

Fan

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…This effect may be mainly reflected in the regulation of non-radical ROS. Sal B can regulate the expression of various antioxidant enzymes, such as increasing the expression of SOD, GSH-Px, and HO-1 (Lee et al, 2014;Zhao et al, 2017), inhibiting the expression of NOX-2 and NOX-4 (Ling et al, 2017), inhibiting the poly (ADP-ribozyme) polymerase 1 (PARP-1) activity to prevent NAD + depletion (Liu et al, 2014) and upregulating Grx1 expression , thereby effectively inhibiting the generation of ROS and reducing the production of lipid peroxidation products such as MDA, to exert an antioxidant effects . In addition, ROS also can activate NF-κB through Toll-like receptor (TLR)4 and TNF-α to promote the expressions of COX2 and NOS, and further promote the generation of ROS .…”

Section: Mechanisms Of Salvianolic Acid B Against Oxidative Damagementioning

confidence: 99%

Pharmacological Effects of Salvianolic Acid B Against Oxidative Damage

Xiao¹,

Liu²,

Mu³

et al. 2020

Front. Pharmacol.

101

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Salvianolic acid B (Sal B) is one of the main active ingredients of Salvia miltiorrhiza, with strong antioxidant effects. Recent findings have shown that Sal B has anti-inflammatory, anti-apoptotic, anti-fibrotic effects and can promote stem cell proliferation and differentiation, and has a beneficial effect on cardiovascular and cerebrovascular diseases, aging, and liver fibrosis. Reactive oxygen species (ROS) include oxygen free radicals and oxygen-containing non-free radicals. ROS can regulate cell proliferation, survival, death and differentiation to regulate inflammation, and immunity, while Sal B can scavenge oxygen free radicals by providing hydrogen atoms and reduce the production of oxygen free radicals and oxygen-containing non-radicals by regulating the expression of antioxidant enzymes. The many pharmacological effects of Sal B may be closely related to its elimination and inhibition of ROS generation, and Nuclear factor E2-related factor 2/Kelch-like ECH-related protein 1 may be the core link in its regulation of the expression of antioxidant enzyme to exert its antioxidant effect. What is confusing and interesting is that Sal B exhibits the opposite mechanisms in tumors. To clarify the specific target of Sal B and the correlation between its regulation of oxidative stress and energy metabolism homeostasis will help to further understand its role in different pathological conditions, and provide a scientific basis for its further clinical application and new drug development. Although Sal B has broad prospects in clinical application due to its extensive pharmacological effects, the low bioavailability is a serious obstacle to further improving its efficacy in vivo and promoting clinical application. Therefore, how to improve the availability of Sal B in vivo requires the joint efforts of many interdisciplinary subjects.

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“…As reported by chemistry research, effective compounds of Danshen are mainly summarized into two categories: lipophilic diterpenoids and watersoluble phenolic acids. The phenolic acids have been identified as natural cardiovascular and cerebrovascular protectants with a variety of pharmacological functions, such as anti-inflammation, antiplatelet aggregation, and antioxidation [36][37][38][39][40][41][42]. These phenolic acids have been accounted for most of the biological activities of Danshen, especially the beneficial impact on ischemia/reperfusion (I/R) damage [43].…”

Section: Introductionmentioning

confidence: 99%

Salvianolic Acid D Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing the Cytoplasmic Translocation and Release of HMGB1-Triggered NF-κB Activation to Inhibit Inflammatory Response

Zhang

Song

Wan

et al. 2020

Mediators of Inflammation

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Inflammatory response participates in the overall pathophysiological process of stroke. It is a promising strategy to develop antistroke drugs targeting inflammation. This study is aimed at investigating the therapeutic effect and anti-inflammatory mechanism of salvianolic acid D (SalD) against cerebral ischemia/reperfusion (I/R) injury. A rat middle cerebral artery occlusion/reperfusion (MCAO/R) injury model was established, and an oxygen-glucose deprivation/reoxygenation (OGD/R) injury model was established in PC12 cells. Neurological deficit score, cerebral infarction, and edema were studied in vivo. Cell viability was achieved using the MTT method in vitro. The Bax, Bcl-2, cytochrome c, HMGB1, TLR4, TRAF6, NF-κB p65, p-NF-κB p65, and cleaved caspase-3 and -9 were tested via the Western blot method. Cytokines and cytokine mRNA, including TNF-α, IL-1β, and IL-6, were studied via ELISA and PCR methods. The translocation of HMGB1 and NF-κB were studied by immunofluorescence assay. The HMGB1/NeuN, HMGB1/GFAP, and HMGB1/Iba1 double staining was carried out to observe the localization of HMGB1 in different cells. Results showed that SalD alleviated neurological impairment, decreased cerebral infarction, and reduced edema in I/R rats. SalD improved OGD/R-downregulated PC12 cell viability. SalD also promoted Bcl-2 expression and suppressed Bax, cytochrome c, and cleaved caspase-3 and -9 expression. SalD decreased the intensity of TLR4, MyD88, and TRAF6 proteins both in vivo and in vitro, and significantly inhibited the NF-κB nuclear translocation induced by I/R and OGD/R. What’s more, SalD inhibited HMGB1 cytoplasmic translocation in neurons, astrocytes, and microglia in both the cortex and hippocampus regions of I/R rats. In conclusion, SalD can alleviate I/R-induced cerebral injury in rats and increase the PC12 cell viability affected by OGD/R. The anti-inflammatory mechanism of SalD might result from the decreased nuclear-to-cytoplasmic translocation of HMGB1 and the inhibition on its downstream TLR4/MyD88/NF-κB signaling.

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Salvianolic acid B attenuates lipopolysaccharide-induced acute lung injury in rats through inhibition of apoptosis, oxidative stress and inflammation

Cited by 33 publications

References 29 publications

Protective functions of salvianolic acid B in PC-12 cells against hydrogen peroxide-triggered damage by mediation of microRNA-26a

Protective functions of salvianolic acid B in PC-12 cells against hydrogen peroxide-triggered damage by mediation of microRNA-26a

Pharmacological Effects of Salvianolic Acid B Against Oxidative Damage

Salvianolic Acid D Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing the Cytoplasmic Translocation and Release of HMGB1-Triggered NF-κB Activation to Inhibit Inflammatory Response

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