Sesamin: A promising protective agent against diabetes-associated cognitive decline in rats

Farbood, Yaghoob; Ghaderi, Shahab; Rashno, Masome; Khoshnam, Seyed Esmaeil; Khorsandi, Layasadat; Sarkaki, Alireza; Rashno, Mohammad

doi:10.1016/j.lfs.2019.05.071

Cited by 35 publications

(30 citation statements)

References 58 publications

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“…Administration of 100 and 200 mg/kg of body weight/day sesamin for 4 weeks to diabetic rats improved blood glucose levels (Thuy et al, 2017). Similar results were seen by supplementing 30 mg/kg/day for 8 weeks in the study of Farbood et al (Farbood et al, 2019). Feeding diabetic rats with a diet consisting of 12% white sesame oil for 60 days caused significant improvement in glucose levels (Aslam et al, 2017).…”

Section: Discussionsupporting

confidence: 83%

Consumption of sesame seeds and sesame products has favorable effects on blood glucose levels but not on insulin resistance: A systematic review and meta‐analysis of controlled clinical trials

Sohouli

Haghshenas

Hernández‐Ruiz³

et al. 2022

Phytotherapy Research

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Sesame, with an oily seed containing oil, lignans, and proteins, is a popular plant that has demonstrated health benefits such as antioxidative, antiobesity, and antiinflammatory effects. In this systematic review and meta-analysis, we aimed to summarize the effect of sesame seeds and their consumption compared to a control group on blood glucose and insulin resistance in human adults. PubMed/MEDLINE, SCOPUS, Web of Science, Google Scholar, and EMBASE were searched to identify eligible controlled clinical trials up to February 2021. Finally, eight clinical trials were included in this study. Sesame products used in these trials were sesame oil, sesamin, and tahini, and the duration of the intervention varied from 45 days to 9 weeks. Our results showed the significant positive effects of sesame and its products on fasting blood glucose FBG (weighted mean difference, WMD: À21.

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Section: Discussionsupporting

confidence: 83%

Consumption of sesame seeds and sesame products has favorable effects on blood glucose levels but not on insulin resistance: A systematic review and meta‐analysis of controlled clinical trials

Sohouli

Haghshenas

Hernández‐Ruiz³

et al. 2022

Phytotherapy Research

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“…It should be noticed that the neurological or cardioprotective actions caused by SSM, SesA, or other structurally similar compounds, as described previously [42,[46][47][48][49][50][51][52][53], can be intimately linked to their direct actions on the amplitude and gating of ion currents (e.g., I Na ). Similar to the ranolazine or perampanel action on I Na described previously [23,25], the inhibitory effect of SSM on ion currents seen herein may be responsible for its wide spectrum of effects observed in vivo [3,54].…”

Section: Discussionmentioning

confidence: 85%

Effects of Sesamin, the Major Furofuran Lignan of Sesame Oil, on the Amplitude and Gating of Voltage-Gated Na+ and K+ Currents

et al. 2020

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Sesamin (SSM) and sesamolin (SesA) are the two major furofuran lignans of sesame oil and they have been previously noticed to exert various biological actions. However, their modulatory actions on different types of ionic currents in electrically excitable cells remain largely unresolved. The present experiments were undertaken to explore the possible perturbations of SSM and SesA on different types of ionic currents, e.g., voltage-gated Na+ currents (INa), erg-mediated K+ currents (IK(erg)), M-type K+ currents (IK(M)), delayed-rectifier K+ currents (IK(DR)) and hyperpolarization-activated cation currents (Ih) identified from pituitary tumor (GH3) cells. The exposure to SSM or SesA depressed the transient and late components of INa with different potencies. The IC50 value of SSM needed to lessen the peak or sustained INa was calculated to be 7.2 or 0.6 μM, while that of SesA was 9.8 or 2.5 μM, respectively. The dissociation constant of SSM-perturbed inhibition on INa, based on the first-order reaction scheme, was measured to be 0.93 μM, a value very similar to the IC50 for its depressant action on sustained INa. The addition of SSM was also effective at suppressing the amplitude of resurgent INa. The addition of SSM could concentration-dependently inhibit the IK(M) amplitude with an IC50 value of 4.8 μM. SSM at a concentration of 30 μM could suppress the amplitude of IK(erg), while at 10 μM, it mildly decreased the IK(DR) amplitude. However, the addition of neither SSM (10 μM) nor SesA (10 μM) altered the amplitude or kinetics of Ih in response to long-lasting hyperpolarization. Additionally, in this study, a modified Markovian model designed for SCN8A-encoded (or NaV1.6) channels was implemented to evaluate the plausible modifications of SSM on the gating kinetics of NaV channels. The model demonstrated herein was well suited to predict that the SSM-mediated decrease in peak INa, followed by increased current inactivation, which could largely account for its favorable decrease in the probability of the open-blocked over open state of NaV channels. Collectively, our study provides evidence that highlights the notion that SSM or SesA could block multiple ion currents, such as INa and IK(M), and suggests that these actions are potentially important and may participate in the functional activities of various electrically excitable cells in vivo.

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“…These studies indicate that independent of ER stress, IRE1α exerts its proapoptotic effect by activating the ASK1-JNK1/2 pathway, supporting the hypothesis that IRE1α activity and ASK1 pathway activation has a reciprocal causal relationship during DICD. Additionally, diabetes-induced oxidative stress in the hippocampus of rats has been previously reported as a factor that contributes to cognitive dysfunction ( Wang et al, 2010 ; Tabatabaei et al, 2017 ; Farbood et al, 2019 ) with evidence of synaptic damage ( Fukui et al, 2001 , 2002 ) and excessive neuronal apoptosis ( Farbood et al, 2019 ; Nazarnezhad et al, 2019 ; Yan et al, 2019 ). The ASK1-JNK1/2 pathway, the important downstream of oxidative stress, may be the major mechanism for oxidative stress-mediated apoptosis during DICD, suggesting that cellular stress does not independently affect DICD development.…”

Section: Discussionmentioning

confidence: 99%

The Reciprocal Causation of the ASK1-JNK1/2 Pathway and Endoplasmic Reticulum Stress in Diabetes-Induced Cognitive Decline

Yuan

et al. 2020

Front. Cell Dev. Biol.

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Diabetes significantly induces cognitive dysfunction. Neuronal apoptosis is the main cause of diabetes-induced cognitive decline (DICD). Apoptosis signal-regulating kinase 1 (ASK1) and endoplasmic reticulum (ER) stress are remarkably activated by diabetes. The role and relationship of ASK1-JNK1/2 signaling and ER stress in DICD have not yet been elucidated. In this study, we used db/db mice as the DICD animal model and confirmed that db/db mice displayed cognitive decline with inferior learning and memory function. Diabetes significantly induced morphological and structural changes, excessive neuronal apoptosis, Aβ 1−42 large deposition, and synaptic dysfunction in the hippocampus. Mechanistic studies found that diabetes significantly triggered ASK1-JNK1/2 signaling activation and increased ER stress in the hippocampus. Moreover, diabetes enhanced the formation of the IRE1α-TRAF2-ASK1 complex, which promotes the crosstalk of ER stress and the ASK1-JNK1/2 pathway during DICD. Furthermore, 4-PBA treatment blocked high glucose (HG)-induced ASK1-JNK1/2 signaling activation, and excessive apoptosis in vitro. Inhibiting ASK1 via siRNA remarkably ameliorated the HG-induced increase in p-IRE1α and associated apoptosis in SH-SY5Y cells, suggesting that ASK1 is essential for the assembly and function of the proapoptotic kinase activity of the IRE1α signalosome. In summary, ER stress and ASK1-JNK1/2 signaling play causal roles in DICD development, which has crosstalk through the formation of the IRE1α-TRAF2-ASK1 complex.

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Sesamin: A promising protective agent against diabetes-associated cognitive decline in rats

Cited by 35 publications

References 58 publications

Consumption of sesame seeds and sesame products has favorable effects on blood glucose levels but not on insulin resistance: A systematic review and meta‐analysis of controlled clinical trials

Consumption of sesame seeds and sesame products has favorable effects on blood glucose levels but not on insulin resistance: A systematic review and meta‐analysis of controlled clinical trials

Effects of Sesamin, the Major Furofuran Lignan of Sesame Oil, on the Amplitude and Gating of Voltage-Gated Na+ and K+ Currents

The Reciprocal Causation of the ASK1-JNK1/2 Pathway and Endoplasmic Reticulum Stress in Diabetes-Induced Cognitive Decline

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