Salidroside alleviates cognitive impairment by inhibiting ferroptosis via activation of the Nrf2/GPX4 axis in SAMP8 mice

Yang, Sixia; Wang, Linshuang; Zeng, Yi Xin; Wang, Yong; Pei, Tingting; Xie, Zeping; Xiong, Qiaowu; Wei, Hui; Li, Wenxu; Li, Jiaqi; Qian, S.; Wei, Dongfeng; Cheng, Wan-Jung

doi:10.1016/j.phymed.2023.154762

Cited by 48 publications

(23 citation statements)

References 46 publications

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“…25−44 The following species were used: C57B mice, SD rats, senescence-resistant mouse 1 (SAMR1) mice, SAMP8 mice, and Kunming (KM) mice. The doses of Sal used were 5,12,20,25,30,40,50,60,75,80,100,120,150, and 180 mg/kg, with one study not specifying the dose administered. The most used animal AD models were models established via D-galactose (D-gal) chemical induction and intracerebroventricular injection of Aβ, and the most involved routes of administration in the studies were oral and i.p.…”

Section: Resultsmentioning

confidence: 99%

“…A total of 20 studies were included. − The following species were used: C57B mice, SD rats, senescence-resistant mouse 1 (SAMR1) mice, SAMP8 mice, and Kunming (KM) mice. The doses of Sal used were 5, 12, 20, 25, 30, 40, 50, 60, 75, 80, 100, 120, 150, and 180 mg/kg, with one study not specifying the dose administered.…”

Section: Resultsmentioning

confidence: 99%

“…37 Using the same AD model, Yang et al found that Sal reduced the expression levels of Aβ 1−42 in a dose-dependent manner. 40 A study using 5× FAD transgenic AD mice found that Sal protected mitochondria and neurons by targeting the NRF2/SIRT3 pathway, attenuated Aβ pathology, improved cognitive function, and could be a potential anti-aging drug candidate. 21 Overall, Sal inhibits the accumulation of Aβ and reduces the neurotoxic effects of Aβ.…”

Section: Discussionmentioning

confidence: 99%

“…Sal can also reduce the levels of soluble and insoluble Aβ in animal models of AD by activating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway, protecting damaged neurons, slowing the pathological progression, and mitigating behavioral symptoms of AD . Using the same AD model, Yang et al found that Sal reduced the expression levels of Aβ 1–42 in a dose-dependent manner . A study using 5× FAD transgenic AD mice found that Sal protected mitochondria and neurons by targeting the NRF2/SIRT3 pathway, attenuated Aβ pathology, improved cognitive function, and could be a potential anti-aging drug candidate .…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotective Mechanisms of Salidroside in Alzheimer’s Disease: A Systematic Review and Meta-analysis of Preclinical Studies

Zhang,

Nao,

Dong

2023

J. Agric. Food Chem.

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Alzheimer’s disease (AD) is a neurodegenerative disease of the central nervous system that occurs in old age and pre-aging, characterized by progressive cognitive dysfunction and behavioral impairment. Salidroside (Sal) is a phenylpropanoid mainly isolated from Rhodiola species with various pharmacological effects. However, the exact anti-AD mechanism of Sal has not been clearly elucidated. This meta-analysis aims to investigate the possible mechanisms by which Sal exerts its anti-AD effects by evaluating behavioral indicators and biochemical characteristics. A total of 20 studies were included, and the results showed that the Sal treatment significantly improved behavior abnormalities in AD animal models. With regard to neurobiochemical indicators, Sal treatment could effectively increase the antioxidant enzyme superoxide dismutase, decrease the oxidative stress indicator malondialdehyde, and decrease the inflammatory indicators interleukin 1β, interleukin 6, and tumor necrosis factor α. Sal treatment was effective in reducing neuropathological indicators, such as amyloid-β levels and the number of apoptotic cells. When the relevant literature on the treatment of rodent AD models is combined with Sal, the therapeutic potential of Sal through multiple mechanisms was confirmed. However, further confirmation by higher quality studies, larger sample sizes, and more comprehensive outcome evaluations in clinical trials is needed in the future.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Neuroprotective Mechanisms of Salidroside in Alzheimer’s Disease: A Systematic Review and Meta-analysis of Preclinical Studies

Zhang,

Nao,

Dong

2023

J. Agric. Food Chem.

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“…Additionally, earlier reports indicated T cells, in particular CD8 + T cells, play an essential role in tumor elimination via identifying tumor‐specific antigens 40,41 . Furthermore, applying SAL might exhibit immunomodulatory effects via inhibiting the infiltration of CD8 + T cells 42,43 . Nevertheless, the role and possible mechanism of SAL on LUAD development and immune escape remain unknown.…”

Section: Discussionmentioning

confidence: 99%

Salidroside suppresses the multiple oncogenic activates and immune escape of lung adenocarcinoma through the circ_0009624‐mediated PD‐L1 pathway

Jin

Chen

et al. 2023

Thoracic Cancer

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BackgroundLung adenocarcinoma (LUAD) is a fatal malignancy all over the world. Salidroside (SAL) is an active component extracted from Rhodiola rosea that has been reported to exert antitumor activity against several human cancers, containing lung adenocarcinoma (LUAD). The purpose of this study was to explore the effect and underlying mechanism of SAL in LUAD.MethodsCell viability, proliferation, migration, and invasion were measured using cell counting kit‐8 (CCK‐8), 5‐ethynyl‐2′‐deoxyuridine (EdU), and transwell assays. Effects of LUAD cells on the cytotoxicity, percentage, and death of CD8+ cells were detected using lactate dehydrogenase (LDH) and flow cytometry assays. Programmed cell death ligand 1 (PD‐L1) protein level was examined using western blot. Circ_0009624, enolase 1 (ENO1), and PD‐L1 levels were determined using real‐time quantitative polymerase chain reaction (RT‐qPCR). The biological role of SAL on LUAD tumor growth was assessed using the xenograft tumor model in vivo.ResultsSAL restrained LUAD cell proliferation, migration, invasion, and immune escape in vitro via modulating PD‐L1. Circ_0009624 expression was increased in LUAD. Applying SAL repressed circ_0009624 and PD‐L1 expression in LUAD cells. SAL treatment hindered suppressed various oncogenic activates and immune escape of LUAD cells by regulating the circ_0009624/PD‐L1 pathway. SAL blocked LUAD xenograft growth in vivo.ConclusionApplying SAL might constrain malignant phenotypes and immune escape of LUAD cells partially through the circ_0009624‐mediated PD‐L1 pathway, providing a novel insight for LUAD treatment.

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Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes

Wang

et al. 2023

Advanced Science

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Emerging evidence suggests that ferroptosis, a unique regulated cell death modality that is morphologically and mechanistically different from other forms of cell death, plays a vital role in the pathophysiological process of neurodegenerative diseases, and strokes. Accumulating evidence supports ferroptosis as a critical factor of neurodegenerative diseases and strokes, and pharmacological inhibition of ferroptosis as a therapeutic target for these diseases. In this review article, the core mechanisms of ferroptosis are overviewed and the roles of ferroptosis in neurodegenerative diseases and strokes are described. Finally, the emerging findings in treating neurodegenerative diseases and strokes through pharmacological inhibition of ferroptosis are described. This review demonstrates that pharmacological inhibition of ferroptosis by bioactive small‐molecule compounds (ferroptosis inhibitors) could be effective for treatments of these diseases, and highlights a potential promising therapeutic avenue that could be used to prevent neurodegenerative diseases and strokes. This review article will shed light on developing novel therapeutic regimens by pharmacological inhibition of ferroptosis to slow down the progression of these diseases in the future.

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Salidroside alleviates cognitive impairment by inhibiting ferroptosis via activation of the Nrf2/GPX4 axis in SAMP8 mice

Cited by 48 publications

References 46 publications

Neuroprotective Mechanisms of Salidroside in Alzheimer’s Disease: A Systematic Review and Meta-analysis of Preclinical Studies

Neuroprotective Mechanisms of Salidroside in Alzheimer’s Disease: A Systematic Review and Meta-analysis of Preclinical Studies

Salidroside suppresses the multiple oncogenic activates and immune escape of lung adenocarcinoma through the circ_0009624‐mediated PD‐L1 pathway

Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes

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