Tanshinone IIA Elicits Neuroprotective Effect Through Activating the Nuclear Factor Erythroid 2-Related Factor-Dependent Antioxidant Response

Cai, Min; Guo, Yongxin; Wang, Shiquan; Wei, Haidong; Sun, Sisi; Zhao, Guangchao; Dong, Hailong

doi:10.1089/rej.2016.1912

Cited by 43 publications

(35 citation statements)

References 34 publications

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“…In this study, Tanshinone IIA preconditioned rats with CIN exhibited lower levels of oxidative stress. The results were consistent with previous studies which focused on Tanshinone IIA for neurologic injury [15]. In the present study, we demonstrated that Tanshinone IIA has protective effects on CIN, and that these protective effects are related, at least in part, to its anti-oxidative properties.…”

Section: Discussionsupporting

confidence: 94%

“…A recent study reported that Tanshinone IIA could up-regulate the expression of Bcl-2, an anti-apoptotic protein [10]. On another hand, it was also reported Nrf2 activation contributed to Tanshinone IIA induced neuroprotection by inducing transcription of large numbers of antioxidant genes including heme oxygenase-1 (HO-1) [15]. We hypothesized that Tanshinone IIA might play the same role in preventing CIN.…”

Section: Discussionmentioning

confidence: 99%

“…Once Nrf2 is activated, it enters the nucleus and binds to antioxidant response elements (AREs), inducing transcription of a large number of antioxidant genes including heme oxygenase-1 (HO-1) [14]. A recent study showed that Nrf2 activation contributes to the neuroprotective effects of Tanshinone IIA during ischemic stroke through its anti-oxidative properties [15]. In the present study, we observed the effects of Tanshinone IIA preteatment on CIN induction, and investigated the underlying mechanism, which we proposed occurred through the Nrf2/ARE pathway.…”

Section: Introductionmentioning

confidence: 99%

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Tanshinone IIA Attenuates Contrast-Induced Nephropathy via Nrf2 Activation in Rats

Liang

Zhao

Cheng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Tanshinone IIA is a chemical compound extracted from Salvia miltiorrhiza Bunge, a perennial plant also known as red sage used in traditional Chinese medicine. Tanshinone IIA has been shown to protect against various organ injuries. In this study, we hypothesized that Tanshinone IIA could play an anti-oxidative role in contrast-induced nephropathy (CIN) through enhancing Nrf2/ARE activation. Methods: To test whether Tanshinone IIA can attenuate CIN, oxidative stress, and apoptosis, we utilized two models: an in vivo Sprague-Dawley rat model of ioversol-induced CIN and an in vitro cell model of oxidative stress in which HK2 cells, a human renal tubular cell line, are treated with hydrogen peroxide (H₂O₂). Rats were randomly assigned to 4 groups (n = 6 per group): control group, ioversol group (ioversol-induced CIN), vehicle group (ioversol-induced CIN rats pretreated with vehicle), and Tanshinone IIA group (ioversol-induced CIN rats pretreated with 25mg/kg Tanshinone IIA). Renal functions, renal injuries and apoptosis were evaluated by using serum creatinine, histological scoring, and TUNEL staning respectively. Malondialdehyde, 8-hydroxy-2’ –deoxyguanosine, and intracellular reactive oxygen species were used for oxidative stress assessment. Levels of Nrf2 and heme oxygenase-1 (HO-1) were measured in vivo and in vitro. Results: Tanshinone IIA attenuated renal tubular necrosis, apoptosis and oxidative stress in rats and oxidative stress in HK2 cells. Furthermore, Tanshinone IIA activated Nrf2, and up-regulated HO-1 expression in vivo and in vitro, resulting in a reduction in oxidative stress. Conclusion: Tanshinone IIA may protect against CIN through enhancing Nrf2/ARE activation.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Tanshinone IIA Attenuates Contrast-Induced Nephropathy via Nrf2 Activation in Rats

Liang

Zhao

Cheng

et al. 2018

Cell Physiol Biochem

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“…Several studies have reported that Tan IIA exhibits antioxidant, anti-inflammatory, and anticancer activities via multiple effects. In acute stress, Tan IIA alleviates the ischemia-reperfusion injury of the heart [ 7 ], liver [ 8 ], brain [ 9 ] and kidneys [ 10 ]. In chronic metabolic disorder, Tan IIA inhibits adipogenic differentiation [ 11 ], fatty liver disease [ 8 ] and diabetic cardiomyopathy [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA reduces SW837 colorectal cancer cell viability via the promotion of mitochondrial fission by activating JNK-Mff signaling pathways

Jieensinue

Zhu

et al. 2018

BMC Cell Biol

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BackgroundMitochondrial homeostasis has been increasingly viewed as a potential target of cancer therapy, and mitochondrial fission is a novel regulator of mitochondrial function and apoptosis. The aim of our study was to determine the detailed role of mitochondrial fission in SW837 colorectal cancer cell viability, mobility and proliferation. In addition, the current study also investigated the therapeutic impact of Tanshinone IIA (Tan IIA), a type of anticancer adjuvant drug, on cancer mitochondrial homeostasis.ResultsThe results of our data illustrated that Tan IIA promoted SW837 cell death, impaired cell migration and mediated cancer proliferation arrest in a dose-dependent manner. Functional investigation exhibited that Tan IIA treatment evoked mitochondrial injury, as witnessed by mitochondrial ROS overproduction, mitochondrial potential collapse, antioxidant factor downregulation, mitochondrial pro-apoptotic protein upregulation, and caspase-9-dependent apoptotic pathway activation. Furthermore, we confirmed that Tan IIA mediated mitochondrial damage by activating mitochondrial fission, and the inhibition of mitochondrial fission abrogated the proapoptotic effects of Tan IIA on SW837 cells. To this end, our results demonstrated that Tan IIA modulated mitochondrial fission via the JNK-Mff pathways. The blockade of the JNK-Mff axis inhibited Tan IIA-mediated mitochondrial fission and promoted the survival of SW837 cells.ConclusionsAltogether, our results identified mitochondrial fission as a new potential target to control cancer viability, mobility and proliferation. Furthermore, our findings demonstrate that Tan IIA is an effective drug to treat colorectal cancer by activating JNK-Mff-mitochondrial fission pathways.Electronic supplementary materialThe online version of this article (10.1186/s12860-018-0174-z) contains supplementary material, which is available to authorized users.

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“…Protective effects were also partly mediated by its anti-inflammatory effect on macrophage migration inhibition factor (MIF) expression, NF-κB activity, the release of proinflammatory cytokines (TNF-α and IL-6), and the reduction of neutrophil infiltration together with antiapoptotic effects by the reduction of caspase-3 expression and increased B-cell lymphoma 2 (bcl-2) protein expression in the ischemic cortex [92]. Nrf2 activation by tanshinone IIA treatment increased the content of antioxidant enzymes and reduced the generation of oxidative products after focal brain ischemia [96]. All these findings suggest great potential of tanshinone IIA in ischemic brain damage.…”

Section: Tanshinonesmentioning

confidence: 99%

Molecular Targets Involved in the Neuroprotection Mediated by Terpenoids

et al. 2019

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Natural products and their derivatives represent the most consistently successful source of drug leads. Terpenoids, a structurally diverse group, are secondary metabolites widely distributed in nature, endowed with a wide range of biological activities such as antibacterial, anti-inflammatory, antitumoral, or neuroprotective effects, which consolidate their therapeutic value. During the last decades, and taking into consideration the prevalence of aging-related diseases, research activity into the neuroprotective effects of these types of compounds has increased enormously. Several signaling pathways involved in neuroprotection are targets of their mechanism of action and mediate their pleiotropic protective activity in neuronal cell damage. In the present review, molecular basis of the neuroprotection exerted by terpenoids is presented, focusing on preclinical evidence of the therapeutic potential of diterpenoids and triterpenoids on neurodegenerative disorders. By acting on diverse mechanisms simultaneously, terpenoids have been emphasized as promising multitarget agents.

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Tanshinone IIA Elicits Neuroprotective Effect Through Activating the Nuclear Factor Erythroid 2-Related Factor-Dependent Antioxidant Response

Cited by 43 publications

References 34 publications

Tanshinone IIA Attenuates Contrast-Induced Nephropathy via Nrf2 Activation in Rats

Tanshinone IIA Attenuates Contrast-Induced Nephropathy via Nrf2 Activation in Rats

Tanshinone IIA reduces SW837 colorectal cancer cell viability via the promotion of mitochondrial fission by activating JNK-Mff signaling pathways

Molecular Targets Involved in the Neuroprotection Mediated by Terpenoids

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