EffectsofLuteolinonLiver,KidneyandBraininPentylentetrazol-Induced Seizures: Involvement of Metalloproteinases and NOS Activities

Birman, Hüsniye; Dar, Kadriye Akgün; Kapucu, Ayşegül; Acar, Samet; Üzüm, Gülay

doi:10.5152/balkanmedj.2011.030

Cited by 16 publications

(7 citation statements)

References 38 publications

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“…It has been shown that epileptic seizures are induced in rats after intraventricular injection with an activated microglia-conditioned medium, suggesting that activation of microglia may also be an important process for the onset of epilepsy [ 79 ]. Accordingly, several studies have shown that pre-treatment with luteolin significantly reduces the frequency of pentylentetrazol-induced seizures in animal models of epilepsy [ 80 – 82 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of microglia overactivation restores neuronal survival in a mouse model of CDKL5 deficiency disorder

Galvani

Mottolese

Gennaccaro

et al. 2021

J Neuroinflammation

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Background CDKL5 deficiency disorder (CDD), a severe neurodevelopmental disorder characterized by early onset epilepsy, intellectual disability, and autistic features, is caused by mutations in the CDKL5 gene. Evidence in animal models of CDD showed that absence of CDKL5 negatively affects neuronal survival, as well as neuronal maturation and dendritic outgrowth; however, knowledge of the substrates underlying these alterations is still limited. Neuroinflammatory processes are known to contribute to neuronal dysfunction and death. Recent evidence shows a subclinical chronic inflammatory status in plasma from CDD patients. However, to date, it is unknown whether a similar inflammatory status is present in the brain of CDD patients and, if so, whether this plays a causative or exacerbating role in the pathophysiology of CDD. Methods We evaluated microglia activation using AIF-1 immunofluorescence, proinflammatory cytokine expression, and signaling in the brain of a mouse model of CDD, the Cdkl5 KO mouse, which is characterized by an impaired survival of hippocampal neurons that worsens with age. Hippocampal neuron survival was determined by DCX, NeuN, and cleaved caspase-3 immunostaining in Cdkl5 KO mice treated with luteolin (10 mg/kg), a natural anti-inflammatory flavonoid. Since hippocampal neurons of Cdkl5 KO mice exhibit increased susceptibility to excitotoxic stress, we evaluated neuronal survival in Cdkl5 KO mice injected with NMDA (60 mg/kg) after a 7-day treatment with luteolin. Results We found increased microglial activation in the brain of the Cdkl5 KO mouse. We found alterations in microglial cell morphology and number, increased levels of AIF-1 and proinflammatory cytokines, and activation of STAT3 signaling. Remarkably, treatment with luteolin recovers microglia alterations as well as neuronal survival and maturation in Cdkl5 KO mice, and prevents the increase in NMDA-induced cell death in the hippocampus. Conclusions Our results suggest that neuroinflammatory processes contribute to the pathogenesis of CDD and imply the potential usefulness of luteolin as a treatment option in CDD patients.

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Section: Discussionmentioning

confidence: 99%

Inhibition of microglia overactivation restores neuronal survival in a mouse model of CDKL5 deficiency disorder

Galvani

Mottolese

Gennaccaro

et al. 2021

J Neuroinflammation

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“…Luteolin exhibit higher superoxide and hydroxyl radical scavenging effects than its glycan luteolin-7-glucoside [45]. Luteolin administration is known to reduce liver fibrosis associated MMP-2 and MMP-9 induced by Pentylentetrazol toxicity [46]. Luteolin is also known to alleviate obesity associated NAFLD in diabetic mice by suppressing conversion of carbohydrates to TG [47].…”

Section: Discussionmentioning

confidence: 99%

Hepato-protective effects of Glossogyne tenuifolia in Streptozotocin-nicotinamide-induced diabetic rats on high fat diet

Shibu

Wang

Hung

et al. 2019

BMC Complement Altern Med

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Background Glossogyne tenuifolia (GT) is a traditional herbal tea in Penghu Island, Taiwan. Its extract is traditionally been used as an antipyretic, hepatoprotective and anti-inflammatory remedy in folk medicine among local residents. The present study investigated whether GT could improve streptozotocin-induced acute liver injury of type 2 diabetes mellitus. Methods Male Wistar rats aged eight weeks were induced to be hyperglycemic by the subcutaneous injection of streptozotocin-nicotinamide (STZ-NA) and a combination of a high-fat diet (HFD) (N group). The animals were given GT extracts at a low dose (50 mg/kg) (L group) or a high dose (150 mg/kg) (H group) or an anti-diabetic drug (acarbose) (P group) in drinking water for 4 weeks. Results The results revealed that STZ-NA increased hepatomegaly, hepatocyte cross-sectional area, hypertrophy-related pathways (IL6/STAT3-MEK5-ERK5, NFATc3, p38 and JNK MAPK), proapoptotic molecules (cytochrome C, cleaved caspase-3), and fibrosis-related pathways (FGF-2, pERK1/2). These pathway components were then expressed at lower levels in the L and H group when compared with the N group. The liver-protective effect of GT in STZ-NA-induced diabetic rats with hyperlipidemia was through an enhancement in the activation of the compensatory PI3K-Akt and Bcl2 survival-related pathway. Conclusion The results demonstrate that the hot water extracts of GT efficiently ameliorates the STZ-NA-induced diabetes associated liver damage in rat models.

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“…An important factor in the pharmacological therapy of this disease is that only 30% of patients do not respond to the therapy. Among the reasons, there are the long-term use and side effects like the hepatotoxicity [ 61 ].…”

Section: Discussionmentioning

confidence: 99%

“…Luteolin (3′,4′,5,7-tetrahydroxyflavone), a flavone contained in chamomile and chrysanthemum, has potent antioxidant, neuroprotective, anxiolytic, and anti-inflammatory properties [ 59 , 60 ] and decreased iNOS levels in PTZ induced seizures. Antioxidant effect of luteolin has not been revealed directly, but the increase of eNOS in brain and other tissues and decrease of iNOS show that luteolin has an indirect antioxidant effect [ 61 ].…”

Section: Flavonoids With Action In the Cnsmentioning

confidence: 99%

The Role of Flavonoids on Oxidative Stress in Epilepsy

Diniz

Silva

Lima-Saraiva

et al. 2015

Oxidative Medicine and Cellular Longevity

123

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Backgrounds. Oxidative stress can result from excessive free-radical production and it is likely implicated as a possible mechanism involved in the initiation and progression of epileptogenesis. Flavonoids can protect the brain from oxidative stress. In the central nervous system (CNS) several flavonoids bind to the benzodiazepine site on the GABAA-receptor resulting in anticonvulsive effects. Objective. This review provides an overview about the role of flavonoids in oxidative stress in epilepsy. The mechanism of action of flavonoids and its relation to the chemical structure is also discussed. Results/Conclusions. There is evidence that suggests that flavonoids have potential for neuroprotection in epilepsy.

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EffectsofLuteolinonLiver,KidneyandBraininPentylentetrazol-Induced Seizures: Involvement of Metalloproteinases and NOS Activities

Cited by 16 publications

References 38 publications

Inhibition of microglia overactivation restores neuronal survival in a mouse model of CDKL5 deficiency disorder

Inhibition of microglia overactivation restores neuronal survival in a mouse model of CDKL5 deficiency disorder

Hepato-protective effects of Glossogyne tenuifolia in Streptozotocin-nicotinamide-induced diabetic rats on high fat diet

The Role of Flavonoids on Oxidative Stress in Epilepsy

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