Acetylshikonin from Zicao attenuates cognitive impairment and hippocampus senescence in d-galactose-induced aging mouse model via upregulating the expression of SIRT1

Li, Qisen; Zeng, Jiacheng; Su, Meiling; He, Yu; Zhu, Bin

doi:10.1016/j.brainresbull.2018.01.007

Cited by 45 publications

(18 citation statements)

References 21 publications

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“…Previous studies have demonstrated that shikonin exerts antibacterial, antitumor, anti-inflammatory and antifibrosis effects (11)(12)(13)(14)(15)(16). Certain studies (16)(17)(18)(19) demonstrated that shikonin improved isoproterenol-induced myocardial injury by inhibiting myocardial fibrosis, inflammation, apoptosis and endoplasmic reticulum stress. Wang et al (13) revealed that shikonin inhibited the occurrence and development of pancreatic cancer via the NF-κB signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Shikonin reduces hepatic fibrosis by inducing apoptosis and inhibiting autophagy via the platelet‑activating factor‑mitogen‑activated protein kinase axis

et al. 2020

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Section: Discussionmentioning

confidence: 99%

Shikonin reduces hepatic fibrosis by inducing apoptosis and inhibiting autophagy via the platelet‑activating factor‑mitogen‑activated protein kinase axis

et al. 2020

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“…A reduction in Sirt1 expression with the progression of aging contributes to the upregulation of oxidative damage ( 31 ). Consequently, Sirt1-activating dietary supplements such as resveratrol, eicosapentaenoic acid, docosahexaenoic acid, and acetylshikonin show anti-aging effects ( 32 , 33 ). Moreover, Sirt1 also plays a protective role against neuroinflammation in brain disease ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Long-Term l-Serine Administration Reduces Food Intake and Improves Oxidative Stress and Sirt1/NFκB Signaling in the Hypothalamus of Aging Mice

Zhou

Zhang

et al. 2018

Front. Endocrinol.

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Serine has recently been shown to reduce oxidative stress and inflammation, which, when occurring in the hypothalamus, contribute to age-related obesity. To explore whether long-term serine administration reduces oxidative stress and body weight in aging mice, various concentrations of l-serine dissolved in water were administered to 18-month-old C57BL/6J mice for 6 months. The results showed that the administration of 0.5% (w/v) l-serine significantly reduced food intake and body weight gain during the experiment. Moreover, the administration of 0.5% l-serine decreased the concentrations of leptin, malondialdehyde, interleukin-1β, and interleukin-6, while it increased those of superoxide dismutase and glutathione, in both the serum and hypothalamus. Reactive oxygen species and the activity of nicotinamide adenine dinucleotide phosphate oxidase were reduced in the hypothalamus of aging mice treated with l-serine as compared with untreated control mice. Additionally, the expression of the leptin receptor increased while the levels of neuropeptide Y and agouti-related protein decreased in mice that had been treated with 0.5% l-serine. The expression of Sirt1 and phosphorylated signal transducers and activators of transcription 3 (pSTAT3) increased, while that of phosphorylated NFκB decreased in the mice treated with 0.5% l-serine. These results indicated that long-term l-serine administration reduces body weight by decreasing orexigenic peptide expression and reduces oxidative stress and inflammation during aging in mice, possibly by modulating the Sirt1/NFκB pathway. Thus, l-serine has the potential to be used in the prevention of age-related obesity.

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“…As an important member of the sirtuin family, Sirt-1 is involved in regulating cell proliferation in many human cells. In AD model animals, overexpression of Sirt-1 slowed cell death, neurodegeneration, and cognitive decline [40,41]. Acetylshikonin, which upregulates Sirt-1, can reduce cognitive dysfunction [42].…”

Section: Discussionmentioning

confidence: 99%

Sirt-1 Regulates Physiological Process and Exerts Protective Effects against Oxidative Stress

Liu

Xia

et al. 2021

BioMed Research International

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Background. Recent studies suggest a correlation between the reduced Sirt-1 expression with Alzheimer’s diseases (AD) and depression, respectively, suggesting a possible pathogenic role of the altered Sirt-1 expression in neuronal degenerative diseases, such as AD and depression. However, the molecular mechanisms underlying how Sirt-1 reduction impairs neuronal functions remain unknown. Methods. We used the SK-N-SH neuroblastoma cells to study the role of Sirt-1 expression on physiological roles in neuronal cells. Gain of Sirt-1 was achieved by transiently transfecting Sirt-1 expression plasmid. Sirt-1-specific shRNA was used to elucidate the role of Sirt-1 loss of function. CCK-8 (Cell Counting Kit-8) assay and flow cytometry were used to evaluate cell proliferation. Semiquantitative western blotting was used to detect relative protein levels. A further luciferase reporter gene assay was employed to examine the effect of Sirt-1 expression on the transcriptional activity of p53. RT-qPCR was used to determine the mRNA levels of p21, Bax, and Bcl-2, which were the downstream target genes of p53. Results. Sirt-1 suppressed the p53 downstream gene p21 transcription, while shRNA-mediated Sirt-1 knockdown resulted in a significant increase in p21 expression, implying a possibility that Sirt-1 promotes neuron proliferation through suppressing p53 transcriptional activity. The mRNA and protein levels of p53 were not affected by the altered Sirt-1 expression, suggesting that Sirt-1 regulates the transcriptional regulatory activity of p53 rather than p53 expression. Indeed, we further confirmed that Sirt-1 appeared to inhibit p53 transcriptional activity by attenuating its acetylation and resulted in a decrease of p53’s binding to the p21 promoter. Overexpressed Sirt-1 scavenged reactive oxygen species (ROS) production in SK-N-SH with H2O2. Knockdown of Sirt-1 presented opposite effect; the addition of EX527 (Sirt-1 inhibitor) increased ROS accumulation. Conclusions. Oxidative stress induces Sirt-1 in neuron cells, and Sirt-1 promotes proliferation in SK-N-SH cells, which protects them from oxidative stress-induced cell death, potentially via suppressing the transcriptional activity of p53. These results provide a molecular explanation underlying how the reduced Sirt-1 potentially causes the AD and depression-related diseases, supporting the idea that Sirt-1 can possibly be used as a diagnostic biomarker and/or therapeutic drug target for the AD and depression-related diseases.

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Acetylshikonin from Zicao attenuates cognitive impairment and hippocampus senescence in d-galactose-induced aging mouse model via upregulating the expression of SIRT1

Cited by 45 publications

References 21 publications

Shikonin reduces hepatic fibrosis by inducing apoptosis and inhibiting autophagy via the platelet‑activating factor‑mitogen‑activated protein kinase axis

Shikonin reduces hepatic fibrosis by inducing apoptosis and inhibiting autophagy via the platelet‑activating factor‑mitogen‑activated protein kinase axis

Long-Term l-Serine Administration Reduces Food Intake and Improves Oxidative Stress and Sirt1/NFκB Signaling in the Hypothalamus of Aging Mice

Sirt-1 Regulates Physiological Process and Exerts Protective Effects against Oxidative Stress

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