Ellagic acid protects against diabetes-associated behavioral deficits in rats: Possible involved mechanisms

Farbood, Yaghoob; Rashno, Masome; Ghaderi, Shahab; Khoshnam, Seyed Esmaeil; Sarkaki, Alireza; Rashidi, Khodabakhsh; Rashno, Mohammad; Badavi, Mohammad

doi:10.1016/j.lfs.2019.03.078

Cited by 55 publications

(28 citation statements)

References 65 publications

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“…HFFD‐fed rats displayed significantly upregulated neuroinflammatory markers (TNF‐α, NF‐κB, and iNOS), oxidative stress, and depressive behavior, besides disturbed metabolic parameters (Youssef et al., 2019). Similarly, STZ‐treated diabetic rats showed elevated pro‐inflammatory mediators (IL‐6, TNF‐α) and neuronal apoptosis in the cerebral cortex and hippocampus (Farbood et al., 2019), and reduced blood SOD levels (Şahin et al., 2019). Neuroinflammation is attributed to cell types: microglia and astrocytes.…”

Section: Physiological Factors That Play Key Roles In the Comorbiditymentioning

confidence: 99%

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Subba

Sandhir

Singh

et al. 2021

Eur J of Neuroscience

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Diabetes increases the likelihood of developing depression and vice versa. Research on this bidirectional association has somewhat managed to delineate the interplay among implicated physiological processes. Still, further exploration is required in this context. This review addresses the comorbidity by investigating suspected common pathophysiological mechanisms. One such factor is psychological stress which disturbs the hypothalamic–pituitary–adrenal axis causing hormonal imbalance. This includes elevated cortisol levels, a common biomarker of both depression and diabetes. Disrupted insulin signaling drives the hampered neurotransmission of serotonin, dopamine, and norepinephrine. Also, adipokine hormones such as adiponectin, leptin, and resistin and the orexigenic hormone, ghrelin, are involved in both depression and T2DM. This disarray further interferes with physiological processes encompassing sleep, the gut–brain axis, metabolism, and mood stability. Behavioral coping mechanisms, such as unhealthy eating, mediate disturbed glucose homeostasis, and neuroinflammation. This is intricately linked to oxidative stress, redox imbalance, and mitochondrial dysfunction. However, interventions such as psychotherapy, physical exercise, fecal microbiota transplantation, and insulin‐sensitizing agents can help to manage the distressing condition. The possibility of glucagon‐like peptide 1 possessing a therapeutic role has also been discussed. Nonetheless, there stands an urgent need for unraveling new correlating targets and biological markers for efficient treatment.

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Section: Physiological Factors That Play Key Roles In the Comorbiditymentioning

confidence: 99%

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Subba

Sandhir

Singh

et al. 2021

Eur J of Neuroscience

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“…Kūmarahou contains ellagic acid that is also been shown to attenuate hyperglycemia potential ( Figure 1B ). Studies of diabetic rats treated with ellagic acid revealed a decrease blood glucose levels confirming the anti-hyperglycemic potential of ellagic acid ( Farbood et al, 2019 ). Furthermore, ellagic acid found in Emblica officinalis was also implicated to anti-diabetic activity in pancreatic β-cells, in vitro and in vivo ( Fatima et al, 2017 ).…”

Section: Potential Anti-diabetic Molecular Modes Of Action Of Selectementioning

confidence: 75%

The Potential of Anti-Diabetic Rākau Rongoā (Māori Herbal Medicine) to Treat Type 2 Diabetes Mellitus (T2DM) Mate Huka: A Review

Koia

Shepherd

2020

Front. Pharmacol.

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T2DM (type 2 diabetes mellitus, or Maōri term "mate huka") is a major long-term health issue in New Zealand particularly among the Maōri community. Non-insulin drugs commonly used in New Zealand for the treatment of T2DM have limits to their efficacy as well as side effects, which are of concern for diabetics. As such, the potential for natural products such as traditional rakau rongoāare of interest for potentially preventing the development of T2DM or improving the treatment of the disease. In particular, antidiabetic effects have been reported for rakau rongoāsuch as karamu, kumarahou, and kawakawa. Natural products have been identified in karamu, kumarahou, and kawakawa that have documented potential effects on glucose metabolism that could contribute to the anti-diabetic effect of these rakau rongoa. As such, this could provide scientific insight into the matauranga (traditional knowledge) developed over generations by Maōri. However, detailed laboratory based and clinical studies would be required to understand and validate these properties of karamu, kumarahou, and kawakawa, and to understand how they can be used in T2DM treatment. Social determinants of indigenous health such as language, culture, traditional knowledge, and identity, are important in understanding the relationship Maōri have with their land and the matauranga they developed of the medicinal properties within their rakau rongoa, over many centuries. Interestingly, traditional Maōri views towards scientific research using animal models to test rakau rongoāare varied but supportive. Furthermore, cultural issues surrounding Maōri mana motuhake (self-determination) of traditional rongoāMaōri healing practices and the inequity faced by many kairongoā(rongoāMaōri practitioners) and tohunga (healers) compared to mainstream health are a current issue within the New Zealand health system. As such, a cultural holistic approach for T2DM care among Maōri would be advantageous. This review will outline the available evidence supporting the anti-diabetic efficacy of karamu, kumarahou, and kawakawa. Currently though there is a lack of molecular research to understand the mechanisms of this efficacy, as such this review will

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“…The mean escape latency and the percentage of time spent in the correct quadrant were calculated and used for statistical analyses. The swimming speed was also recorded to assess whether the group differences in escape latency were due to their differences in swimming ability (Farbood et al, 2019;Kiray, Bagriyanik, Pekcetin, Ergur, & Uysal, 2008;Sarkaki et al, 2019).…”

Section: Morris Water Maze (Mwm) Testmentioning

confidence: 99%

Neuroprotective Effects of Chrysin Mediated by Estrogenic Receptors Following Cerebral Ischemia and Reperfusion in Male Rats

Shooshtari

Farbood

Mansouri

et al. 2021

BCN

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Introduction: Ischemic stroke is one of the leading causes of morbidity and mortality worldwide. Neuroprotective strategies were reported to attenuate cognitive deficits after ischemic incidents. Here we studied the neuroprotective potential of chrysin in a rat model of cerebral Ischemia/Reperfusion (I/R) in the presence or absence of Estrogen Receptors (ERs). Methods: Adult male Wistar rats were pretreated with chrysin (CH) (CH; 30 mg/kg; gavage; for 21 consecutive days) alone or with selective ERs antagonists (ERα antagonist MPP; ERβ antagonist PHTPP; IP) or nonselective ERs antagonist (ICI182780; IP). Then, the bilateral common carotid arteries were occluded for 20 min, which was followed by 72 h reperfusion. Subsequently, cognitive performance was evaluated by Morris Water Maze (MWM) and shuttle box tasks, and afterward, their hippocampi were removed for ELISA assays and H&E staining. Oxidative indicators Malondialdehyde (MDA) and Glutathione Peroxidase (GPx), as well as inflammation mediators interleukin (IL)-1β and tumor necrosis factor-alpha (TNFα), were measured using commercial kits. Results: Results of the current study showed that the anti-oxidative and anti-inflammatory properties of CH are possible mechanisms that could improve cognitive deficits and prevent neuronal cell death following I/R (P<0.001). These effects were reversed by ICI182780 (P>0.05). Furthermore, when chrysin was co-treated with ERβ antagonist, PHTPP showed a weak neuroprotective effect in I/R rats. However, these parameters were not significantly different when chrysin was combined with ERα antagonist MPP. Conclusion: Our data confirm that chrysin could potentially serve as a neuroprotective agent against devastating effects of cerebral I/R injury, which may be mediated via its interaction with ERs, especially ERβ.

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Ellagic acid protects against diabetes-associated behavioral deficits in rats: Possible involved mechanisms

Cited by 55 publications

References 65 publications

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

The Potential of Anti-Diabetic Rākau Rongoā (Māori Herbal Medicine) to Treat Type 2 Diabetes Mellitus (T2DM) Mate Huka: A Review

Neuroprotective Effects of Chrysin Mediated by Estrogenic Receptors Following Cerebral Ischemia and Reperfusion in Male Rats

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