Glycyrrhizic acid and silymarin alleviate the neurotoxic effects of aluminum in rats challenged with fructose-induced insulin resistance: possible role of toll-like receptor 4 pathway

Ali, Noura; Mahmoud, A. A.; Mahmoud, Mona F.; Fayoumi, Hassan M. El

doi:10.1080/01480545.2018.1544984

Cited by 21 publications

(18 citation statements)

References 67 publications

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“…In the existing study, intoxication of rats with AlCl 3 markedly elevated TNF-α and IL-1β in the hippocampal tissues, suggesting that AlCl 3 preferentially affects macrophage functions and stimulates the development of brain injury. Our results are compatible with the previous studies reporting neuroinflammation following exposure to Al [ 48 , 49 ]. Nuclear factor-kappa B (NF-κB) is a protein complex that plays a pivotal role in the activation of the neuroinflammatory cascade causing transcription of IL-1β and TNF-α [ 50 ].…”

Section: Discussionsupporting

confidence: 93%

The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats

et al. 2020

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Alzheimer’s disease (AD) is a worldwide rapidly growing neurodegenerative disease. Here, we elucidated the neuroprotective effects of silymarin (SM) on the hippocampal tissues of aluminum chloride (AlCl3)-induced Alzheimer-like disease in rats using biochemical, histological, and ultrastructural approaches. Forty rats were divided into control, SM, AlCl3, and AlCl3 + SM groups. Biochemically, AlCl3 administration resulted in marked elevation in levels of lipid peroxidation (LPO) and nitric oxide (NO) and decrease in levels of reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Moreover, AlCl3 significantly increased tumor necrosis factor-α (TNF-α), interleukin-1beta (IL-1β), and acetylcholinesterase (AChE) activities. Furthermore, myriad histological and ultrastructural alterations were recorded in the hippocampal tissues of AlCl3-treated rats represented as marked degenerative changes of pyramidal neurons, astrocytes, and oligodendrocytes. Additionally, some myelinated nerve fibers exhibited irregular arrangement of their myelin coats, while the others revealed focal degranulation of their myelin sheaths. Severe defects in the blood–brain barrier (BBB) were also recorded. However, co-administration of SM with AlCl3 reversed most of the biochemical, histological, and ultrastructural changes triggered by AlCl3 in rats. The results of the current study indicate that SM can potentially mend most of the previously evoked neuronal damage in the hippocampal tissues of AlCl3-kindled rats.

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Section: Discussionsupporting

confidence: 93%

The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats

et al. 2020

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“…VPA-induced high TG level may be attributed to inhibition of endothelial lipoprotein lipase activity responsible for the hydrolysis of TG. In a study of rats, Ali et al (2019) shows that giving FRAL (fructose (10%) in drinking water plus AlCl3 (34 mg/kg/day)) significantly increased serum TG level to normal rats. FRAL + SLY (100 mg/kg/day) per oral gavage administration resulted in a significant decrease in serum TG level compared to FRAL + SLY.…”

Section: Histopathological Resultsmentioning

confidence: 99%

Sıçanlarda Silimarinin Beyin Hasarı Üzerine Koruyucu Etkisi

Aktaş

Sevimli²

2020

Van Veterinary Journal

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In this study, we evaluated the possible protective effects of silymarin on valproic acid-induced brain injury by histological and biochemical parameters in rats. The experiment was performed with 21 Sprague Dawley male rats. Rats were divided into three groups: group 1 control, group 2 valproic acid and group 3 valproic acid + silymarin. The groups received valproic acid 500 mg/kg/day and silymarin 100 mg/kg/day for 14 days except the control group. Increased serum glucose, cholesterol, triglyceride and creatine kinase BB levels with valproic acid were reversed with silymarin administration. Also, increased malondialdehyde and decreased glutathione levels in brain tissue with valproic acid were significantly suppressed by silymarin. In the valproic acid + silymarin group, oxidative stress was decreased, antioxidant activity was increased and histopathological changes were decreased compared to the valproic acid group. Brain injury caused by valproic acid was attenuated by silymarin treatment owing to the antioxidative and anti-apoptotic effects of silymarin. Silymarin may be useful for reducing the severity of valproic acid induced brain damage.

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“…Paeoniflorin also alleviates okadinic acid induced damage of SH-SY5Y cells by interfering with the Akt/GSK-3 β -related pathway and alleviates the microtubule structure system stress response induced by okadinic acid [ 44 ]. Glycyrrhizic acid had a significant effect on insulin resistance in rats [ 45 ]. It also exerts an anti-neurotoxic effect in the SH-SY5Y cell injury model induced by autophagy 6-hydroxydopamine and corticosterone [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Shenzhiling Oral Liquid Protects STZ‐Injured Oligodendrocyte through PI3K/Akt‐mTOR Pathway

Liu

Qin

Mana

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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White matter degeneration and demyelination are nonnegligible pathological manifestations of Alzheimer’s disease (AD). The damage of myelin sheath consisting of oligodendrocytes is the basis of AD’s unique early lesions. Shenzhiling oral liquid (SZL) was the effective Chinese herbal compound approved by the Food and Drug Administration (FDA) for the treatment of AD in China, which plays the exact therapeutic role in clinical AD patients. However, its molecular mechanism remains unclear to date. For this purpose, an in vitro mode of streptozotocin- (STZ-) induced rat oligodendrocyte OLN-93 cell injury was established to mimic the pathological changes of myelin sheath of AD and investigate the mechanism of SZL protecting injured OLN-93 cell. The results showed that STZ can decrease cell viability and downregulate the activity of PI3K/Akt-mTOR signalling pathway and the expression of myelin sheath-related proteins (MBP, MOG, and PLP) in OLN-93 cells. Both SZL-medicated serum and donepezil (positive control) can protect cells from STZ-caused damage. SZL-medicated serum increased OLN-93 cell viability in a dose- and time-dependent manner and enhanced the activity of PI3K/Akt-mTOR signalling pathway. The inhibitor of PI3K (LY294002) inhibited the protective effect of SZL-medicated serum on the STZ-injured OLN-93 cells. Furthermore, rapamycin, the inhibitor of mTOR, inhibited the promotion of cell viability and upregulation of p-mTOR and MBP caused by SZL-medicated serum. In conclusion, our data indicate that SZL plays its therapeutic role on AD by promoting PI3K/Akt-mTOR signalling pathway of oligodendrocytes. Thus, the present study may facilitate the therapeutic research of AD.

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Glycyrrhizic acid and silymarin alleviate the neurotoxic effects of aluminum in rats challenged with fructose-induced insulin resistance: possible role of toll-like receptor 4 pathway

Cited by 21 publications

References 67 publications

The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats

The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats

Sıçanlarda Silimarinin Beyin Hasarı Üzerine Koruyucu Etkisi

Shenzhiling Oral Liquid Protects STZ‐Injured Oligodendrocyte through PI3K/Akt‐mTOR Pathway

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