Luteoloside attenuates neuroinflammation in focal cerebral ischemia in rats via regulation of the PPARγ/Nrf2/NF-κB signaling pathway

Li, Qiaoling; Tian, Zhichao; Wang, Minghui; Kou, Jiejian; Wang, Chunli; Rong, Xuli; Li, Jing; Xie, Xinmei; Pang, Xiaobin

doi:10.1016/j.intimp.2018.11.044

Cited by 97 publications

(61 citation statements)

References 38 publications

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“…Cerebral ischemia reperfusion (I/ R) leads to the imbalance of brain energy, which is characterized by an insufficient oxygen supply and restoration of blood flow, meanwhile involves complex and multi-factorial mechanism, and further causes cerebral injury including neuroinflammation, neuronal damage, and cerebral edema (Zhou et al, 2017). Due to narrow therapeutic time window, the options for acute ischemia remain very limited, and few neuroprotective treatments have been successfully developed to prevent ischemic injury (Li Q. et al, 2019). I/R results in irreversible damage to brain tissue as well as subsequent disability and a high morbidity to patients.…”

Section: Introductionmentioning

confidence: 99%

Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis

et al. 2020

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The aim of this research is to investigate the potential neuro-protective effect of kaempferol which with anti-oxidant, anti-inflammatory, and immune modulatory properties, and understand the effect of kaempferol on reducing cerebral ischemia reperfusion (I/R) injury in vivo. Male adult Sprague Dawley (SD) rats were pretreated with kaempferol for one week via gavage before cerebral I/R injury operation. We found that kaempferol treatment can reduce the cerebral infarct volume and neurological score after cerebral I/R. Rats were sacrificed after 24 h reperfusion. We observed that kaempferol improved the arrangement, distribution, and morphological structure of neurons, as well as attenuated cell apoptosis in brain tissue via hematoxylin and eosin (H&E) staining, Nissl staining and TUNEL staining. Superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH) kit analysis, enzyme-linked immunosorbent (ELISA) assay, real-time PCR, Western blot, and immunohistochemical examination indicated that kaempferol mitigated oxidative and inflammatory stress via regulating the expression of proteins, p-Akt, p-GSK-3b, nuclear factor erythroid2-related factor 2 (Nrf-2), and p-NF-kB during cerebral I/R, thus increasing the activity of SOD and GSH, meanwhile decreasing the content of MDA in serum and brain tissue, as well as restoring the expression levels of tumor necrosis factor alpha (TNF-a), interleukin-1b (IL-1b), and IL-6 in vivo. Taken together, this study suggested that kaempferol protects against cerebral I/R induced brain damage. The possible mechanism is related with inhibiting oxidative and inflammatory stress induced apoptosis.

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Section: Introductionmentioning

confidence: 99%

Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis

et al. 2020

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“…Some reports have found that luteoloside and celecoxib both have COX-2-independent effects on the signal pathways, such as MAPK/p38, and ERK. (Wu et al, 2004;Hua et al, 2005;Ha et al, 2006;Kadam et al, 2007;Park et al, 2010;Wang et al, 2013;Akram et al, 2015;Jeon et al, 2015;Li et al, 2019;Shao et al, 2018). Although these results have not been applied to studies about analgesic effects, these mechanisms may be the reason of the synergistic effect in the acute analgesic role due to the critical role of MAPK/p38 and ERK signal pathways in the pain regulation.…”

Section: Discussionmentioning

confidence: 99%

Luteoloside Exerts Analgesic Effect in a Complete Freund’s Adjuvant-Induced Inflammatory Model via Inhibiting Interleukin-1β Expression and Macrophage/Microglia Activation

Shi

Zhao

et al. 2020

Front. Pharmacol.

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Background: Flavonoid monomers are proved to have an anti-inflammatory effect and may also be promising for chronic pain treatment. In the present study, the analgesic effect and the relevant mechanisms of luteoloside, one of the flavonoid monomers, were investigated. Methods: The analgesic effect of luteoloside was first evaluated in complete Freud's adjuvant induced inflammatory model by von Frey test and Hargreaves test in both male and female mice. The interleukin-1b levels in plantar tissue, serum, dorsal root ganglion, and the dorsal horn of the spinal cord were determined by enzyme-linked immunosorbent assay or immunofluorescence. The activation of macrophage/microglia was tested by Iba-1 staining. Results: Our data showed that luteoloside exhibited both acute and chronic analgesic phenotypes. Every single dose of luteoloside solution reached the peak transient analgesic effect 2 h after administration and lasted less than 6 h. About 14 consecutive days administration (one dose per day) later, luteoloside showed a sustained analgesic effect which lasted more than 24 h. Celecoxib 20 mg/kg combined with luteoloside 40 mg/kg achieved a similar analgesic effect as celecoxib 40 mg/kg alone. Luteoloside inhibited interleukin-1b expression in plantar tissue, dorsal root ganglion, the dorsal horn of spinal cord, and serum, after 14 days of continuous administration. Furthermore, our results also showed that the activation of macrophage/microglia in dorsal root ganglions were significantly inhibited 2 h after each single dose in daily luteoloside administration and recovered to a higher level 6 h later. These findings might be involved in the mechanisms of the acute analgesic effect of luteoloside.

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“…They found that the NF‐kB protein expression increased in lippolisaccharide group but the NF‐kB protein expression decreased with the pomegranate juice application. Li et al (2019) investigated the protective effect of Lutecoside on cerebral ischemia. They found that the COX‐2 protein expression significantly increased in rats cured with medium cerebral artery occlusion (MCAO) in comparison to the control group and additionally the Nrf‐2 protein expression levels of cerebral homogenate increased significantly with luteoloside treatment.…”

Section: Discussionmentioning

confidence: 99%

The preventive effect of ellagic acid on brain damage in rats via regulating of Nrf‐2, NF‐kB and apoptotic pathway

et al. 2020

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The aim of this study was to investigate the neuroprotective role of ellagic acid (EA) on CCl4‐induced brain injury in rats. In this study, the rats were divided into four groups. Groups: (1) Control group; (2) EA group; (3) CCl4 group; (4) EA + CCl4 group. In brain tissue, tumor necrosis factor‐α (TNF‐α), nuclear factor kappa b (NF‐kB), cyclooxygenase‐2 (COX‐2), nuclear erythroid related factor 2 (Nrf‐2), cysteine‐aspartic acid protease (caspase‐3), VEGF (vascular endothelial growth factor) and B‐cell lymphoma‐2 (bcl‐2) protein expression levels were analyzed by western blotting. MDA (malondialdehyde), catalase enzyme activity (CAT) and glutathione (GSH) analysis were determined by spectrophotometer. In our findings, EA ameliorated Nrf‐2 and caspase‐3 protein expression levels, GSH and catalase activities, NF‐kB, TNF‐α, VEGF, Bcl‐2, COX‐2 protein expression levels and MDA levels in CCl4 intoxicated rats. These results suggest that EA demonstrated the neuroprotective effect on CCl4‐induced brain damage in rats. Practical applications Ellagic acid has different biological activities, these are; antioxidant, anti‐inflammatory, antidepressant, antifibrosis, anticancer, neuroprotective and hepatoprotective. For example it was reported that EA protects the cells against DNA injury induced by free radicals and it can prevent the traumatic brain injury. These results obtained from this study reveals that EA has a protective effect against rat brain damage and it may be used as an alternative drugs for the brain injury treatment in future.

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Luteoloside attenuates neuroinflammation in focal cerebral ischemia in rats via regulation of the PPARγ/Nrf2/NF-κB signaling pathway

Cited by 97 publications

References 38 publications

Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis

Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis

Luteoloside Exerts Analgesic Effect in a Complete Freund’s Adjuvant-Induced Inflammatory Model via Inhibiting Interleukin-1β Expression and Macrophage/Microglia Activation

The preventive effect of ellagic acid on brain damage in rats via regulating of Nrf‐2, NF‐kB and apoptotic pathway

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