Neurodegenerative changes and neuroapoptosis induced by systemic lipopolysaccharide administration are reversed by dexmedetomidine treatment in mice

Ning, Qiaoqing; Liu, Zhaoguo; Wang, Xiuhua; Zhang, Ruyi; Yang, Meizi; Sun, Hongliu; Han, Fang; Zhao, Wenxiang; Zhang, Xiuli

doi:10.1080/01616412.2017.1281197

Cited by 74 publications

(48 citation statements)

References 59 publications

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“…Numerous studies have revealed that dysfunction of the BBB may lead to brain edema, destruction of the cerebral microenvironment and subsequent brain damage (19,30). Consequently, BBB dysfunction has been proposed to represent an important factor associated with the development of PE (19,20,30). In the present study, decreased levels of EB extravasation suggested that berberine has a protective effect against BBB dysfunction.…”

Section: Discussionsupporting

confidence: 49%

“…Inf lammation is an important factor involved in sepsis-associated encephalopathy, which is strongly associated with neuronal apoptosis (20,31). Another form of programmed cell death, necroptosis (32), which is strongly associated with inflammation, shares common morphological features with apoptosis and is tightly regulated by kinases, such as RIP1 and RIP3 (33).…”

Section: Discussionmentioning

confidence: 99%

“…4B and C). (20,21). To further investigate the hippocampus-dependent memory impairment exhibited by rats in the SAP group, as demonstrated by the aforementioned FCT, western blotting was performed to determine the expression levels of proteins associated with apoptosis and necroptosis in hippocampal tissues (Fig.…”

Section: Berberine Attenuates Cognitive Deficits In Sap Ratsmentioning

confidence: 99%

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Cognitive impairments induced by severe acute pancreatitis are attenuated by berberine treatment in rats

Hua

Liao

et al. 2018

Mol Med Report

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Cognitive impairments induced by severe acute pancreatitis (SAP) are severe complications, for which there are a lack of effective pharmacological treatment strategies. Berberine is an isoquinoline alkaloid extracted from the Chinese herb, Coptis rhizome, which exhibits numerous biological effects on gastrointestinal disorders. However, the effects of berberine on SAP‑induced cognitive impairments remain unknown. The present study aimed to investigate the effects of berberine on cognitive impairments associated with SAP. Wistar rats were randomly divided into Sham, Sham + berberine, SAP and SAP + berberine groups. Rats were intraperitoneally injected with L‑arginine (3 g/kg) to induce SAP. Subsequently, selected rats were intragastrically administered berberine (100 mg/kg) once daily for 6 consecutive days. Disease severities of rats were investigated 48 h post‑induction of SAP via determination of serum amylase levels and hematoxylin and eosin staining. Survival rates, performance of behavioral tests (automated rotarod and fear conditioning tests), blood brain barrier (BBB) permeability, and the expression levels of tumor necrosis factor (TNF)‑α and interleukin (IL)‑1β in hippocampal tissues were also determined. Proteins associated with apoptosis and necroptosis in the hippocampal tissues of SAP rats, including caspase‑3, receptor‑interacting protein kinase (RIP)1 and RIP3, were detected via western blotting. The results revealed that treatment with L‑arginine induced SAP, which subsequently resulted in increased BBB permeability, mortality rates and cognitive deficits in rats. The expression levels of TNF‑α, IL‑1β, caspase‑3, RIP1 and RIP3 were significantly increased in the hippocampal tissues of SAP rats, thus suggesting that neuroinflammation, apoptosis and necroptosis may be involved in neurodegeneration associated with the development of SAP. Notably, administration of berberine protected the integrity of the BBB, decreased levels of brain inflammation and mortality rates, and attenuated increased levels of proteins associated with apoptosis and necroptosis and cognitive deficits associated with SAP in rats. The results of the present study demonstrated that daily treatment with berberine may attenuate cognitive deficits and reduce associated mortality via exhibition of anti‑neuroinflammatory effects and attenuation of neuronal apoptosis and necroptosis in the hippocampal tissues of SAP rats.

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Section: Discussionsupporting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

Section: Berberine Attenuates Cognitive Deficits In Sap Ratsmentioning

confidence: 99%

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Cognitive impairments induced by severe acute pancreatitis are attenuated by berberine treatment in rats

Hua

Liao

et al. 2018

Mol Med Report

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“…Also, they reported that interleukin 6 levels in brain tissue are not significantly changed after 24 h. In the literature, TNF-alpha was commonly measured as a marker for sepsis associated encephalopathy in the brain tissue. The interleukin 6 levels were measured in serum [1,19,21–24]. …”

Section: Discussionmentioning

confidence: 99%

Effects of Ecballium elaterium on brain in a rat model of sepsis-associated encephalopathy

Arslan

Ekinci

Arıcı

et al. 2017

Libyan Journal of Medicine

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Despite recent advances in antibiotic therapy, sepsis remains a major clinical challenge in intensive care units. Here we examined the anti-inflammatory and antioxidant effects of Ecballium elaterium (EE) on brain, and explored its therapeutic potential in an animal model of sepsis-associated encephalopathy (SAE) [induced by cecal ligation and puncture (CLP)].Thirty rats were divided into three groups of 10 each: control, sepsis, and treatment. Rats were subjected to CLP except for the control group, which underwent laparatomy only. The treatment group received 2.5 mg/kg EE while the sepsis group was administered by saline. Twenty-four hours after laparotomy, animals were sacrificied and the brains were removed. Brain homogenates were prepared to assess interleukin 1beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), total antioxidant capacity (TAC), and total oxidant status (TOS). Brain tissue sections were stained by hematoxylin and eosin (H&E) to semi-quantitatively examine the histopathologic changes such as neuron degeneration, pericellular/perivascular edema and inflammatory cell infiltration in the cerebral cortex.We found a statistically significant reduction in brain tissue homogenate levels of TNF-α 59.5 ± 8.4/50.2 ± 6.2 (p = 0.007) and TOS 99.3 ± 16.9/82.3 ± 7.8 (p = 0.01) in rats treated with EE; although interleukin 6 levels were increased in the treatment group compared to the sepsis group, this was not statistically significant. Neuronal damage (p = 0.00), pericellular/perivascular edema and inflammatory cell infiltration (p = 0.001) were also significantly lower in the treatment group compared to those in the sepsis group.These data suggest that Ecballium elaterium contains some components that exert protective effects against SAE in part by attenuating accumulation of proinflammatory cytokines, which may be important contributors to its anti-inflammatory effects during sepsis.

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“…13,14 Studies have shown that agents that control the apoptotic pathways and reduce the number of apoptotic neurons might provide a therapeutic approach against SAE. 15,16 …”

Section: Introductionmentioning

confidence: 99%

Sevoflurane exerts brain-protective effects against sepsis-associated encephalopathy and memory impairment through caspase 3/9 and Bax/Bcl signaling pathway in a rat model of sepsis

et al. 2018

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ObjectiveWe compared the effects of sevoflurane and isoflurane on systemic inflammation, sepsis-associated encephalopathy, and memory impairment in a rat sepsis model of cecal ligation and puncture (CLP)-induced polymicrobial peritonitis.MethodsTwenty-four rats were assigned to sham, CLP, CLP + sevoflurane, and CLP + isoflurane groups. At 72 hours after CLP, the rats underwent behavior tests. Serum cytokines were evaluated. Brain tissue samples were collected for determination of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase; the wet/dry weight ratio; myeloperoxidase (MPO) and malondialdehyde (MDA); apoptotic gene release; and histologic examinations.ResultsThe MPO level, wet/dry weight ratio, and histopathology scores were lower and the Bcl2a1 and Bcl2l2 expressions were upregulated in both the CLP + sevoflurane and CLP + isoflurane groups compared with the CLP group. The interleukin-6, interleukin-1β, MDA, and caspase 3, 8, and 9 levels were lower; the GPX, SOD, Bax, Bcl2, and Bclx levels were higher; and non-associative and aversive memory were improved in the CLP + sevoflurane group compared with the CLP + isoflurane group.ConclusionSevoflurane decreased apoptosis and oxidative injury and improved memory in this experimental rat model of CLP. Sevoflurane sedation may protect against brain injury and memory impairment in septic patients.

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Neurodegenerative changes and neuroapoptosis induced by systemic lipopolysaccharide administration are reversed by dexmedetomidine treatment in mice

Abstract: Our results indicated that Dex could reverse neurodegenerative changes and neuroapoptosis in mice brain of septic mice induced by LPS through anti-inflammatory and antiapoptotic effects.

Cited by 74 publications

References 59 publications

Cognitive impairments induced by severe acute pancreatitis are attenuated by berberine treatment in rats

Cognitive impairments induced by severe acute pancreatitis are attenuated by berberine treatment in rats

Effects of Ecballium elaterium on brain in a rat model of sepsis-associated encephalopathy

Sevoflurane exerts brain-protective effects against sepsis-associated encephalopathy and memory impairment through caspase 3/9 and Bax/Bcl signaling pathway in a rat model of sepsis

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