Cistanches alleviates sevoflurane‐induced cognitive dysfunction by regulating PPAR‐γ‐dependent antioxidant and anti‐inflammatory in rats

Peng, Sheng; Li, Pengyi; Liu, Peirong; Yan, Huixin; Wang, Juan; Lü, Weihua; Liu, Chunliang; Zhou, Yixin

doi:10.1111/jcmm.14807

Cited by 40 publications

(25 citation statements)

References 48 publications

(160 reference statements)

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“…The appropriate management of pre-existing diseases and maintenance of optimum bodily functioning may be an effective way to reduce the incidence of sevoflurane-induced POCD. Finally, in older animals, postanaesthetic sevoflurane-related behavioral deficits tend to be larger and last longer than those in younger animals ( Peng et al, 2020 ).Therefore, it is important that studies include aged rodents when performed to investigate the mechanism of sevoflurane-induced POCD.…”

Section: Sevoflurane-inhalation Anesthesiamentioning

confidence: 99%

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Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Wang

Chen

Zhang

et al. 2021

Front. Aging Neurosci.

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Sevoflurane is one of the most widely used anesthetics for the induction and maintenance of general anesthesia in surgical patients. Sevoflurane treatment may increase the incidence of postoperative cognitive dysfunction (POCD), and patients with POCD exhibit lower cognitive abilities than before the operation. POCD affects the lives of patients and places an additional burden on patients and their families. Understanding the mechanism of sevoflurane-induced POCD may improve prevention and treatment of POCD. In this paper, we review the diagnosis of POCD, introduce animal models of POCD in clinical research, analyze the possible mechanisms of sevoflurane-induced POCD, and summarize advances in treatment for this condition.

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Section: Sevoflurane-inhalation Anesthesiamentioning

confidence: 99%

“…Cistanches . can regulate PPAR-γ-dependent antioxidative and anti-inflammatory effects in rats ( Peng et al, 2020 ). Both resveratrol and Cistanches have been proven to reduce sevoflurane neurotoxicity in rats.…”

Section: Advances In Treatmentmentioning

confidence: 99%

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Wang

Chen

Zhang

et al. 2021

Front. Aging Neurosci.

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“…In recent years, some reports suggested that Sev could induce neuronal apoptosis and the resulting neurotoxicity is attributed to cognitive impairment like POCD in the elderly animal models [ 1 , 9 , 10 ]. In addition, a few researches showed that reactive oxygen species (ROS) and neuroinflammation [ 11 , 12 – 15 ] were closely related to the pathogenesis of POCD. Despite more than 20 years of intensive research and the fact that some signaling pathways were discovered, most details and exact mechanisms about POCD remain unclear.…”

Section: Introductionmentioning

confidence: 99%

A new mechanism of POCD caused by sevoflurane in mice: cognitive impairment induced by cross-dysfunction of iron and glucose metabolism

Zuo

Jinhong

et al. 2021

Aging

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Sevoflurane (Sev) is a commonly used anesthetic in hospitals that can cause neurotoxicity. Postoperative cognitive dysfunction (POCD) is a common clinical problem induced by some anesthetics. However, the exact mechanism of neurotoxicity induced by Sev is unclear. Here we studied a new mechanism of POCD induced by Sev. We treated 15-month-old mice with 2% Sev for 6 hours, and we had found that Sev causes POCD. Using isobaric tags for relative and absolute quantitation (iTRAQ), we found that the transporter and the metabolism of carbohydrates and inorganic ions were involved in the cognitive impairment induced by Sev. Using synchrotron radiation micro-X-ray fluorescence (μ-XRF), we showed that Sev caused the iron overload in the brain of 15-month-old mice. Subsequently, excessive iron led to oxidative stress and impaired mitochondrial function that further led to glucose metabolism disorder and reduced ATP production by regulating the expression of key enzyme genes or proteins including G6Pase, Pck1, and Cs. Meanwhile, Sev also inhibited the oxygen consumption rate and glucose absorption by downregulating the expression of glucose transporter 1 in cerebral vascular endothelial cells. The cross-dysfunction of iron and glucose metabolism caused the apoptosis in the cortex and hippocampus through Bcl2/Bax pathway. In conclusion, the data here showed a new mechanism that Sev caused apoptosis by cross-dysregulation of iron and glucose metabolism and induced energy stress in mice. Maintaining iron and glucose metabolism homeostasis may play an important role in cognitive impairment induced by Sev.

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“…Previous research has confirmed that PPARγ possessed potent effects of anti-inflammatory and antioxidative 32 , 33 . Thus, we speculated that PPARγ related to the protective effects of licochalcone A against LPS-induced inflammatory dermal cells.…”

Section: Discussionmentioning

confidence: 89%

The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide

Tian

Liu

et al. 2022

Sci Rep

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Laminitis is one of the most important and intractable diseases in dairy cows, which can lead to enormous economic losses. Although many scholars have conducted a large number of studies on laminitis, the therapeutic test of medicinal plants in vitro is really rare. Licochalcone A is proved to possess anti-inflammatory and anti-oxidant properties. But the effect of licochalcone A on LPS-induced inflammatory claw dermal cells has not been discovered yet. In this study, the primary dairy cow claw dermal cells were treated with gradient concentrations of licochalcone A (1, 5, 10 µg/mL) in the presence of 10 µg/mL lipopolysaccharides (LPS). The results indicated that licochalcone A reduced the concentrations of inflammation mediators (TNF-α, IL-1β and IL-6), increased the activity of SOD, reduced the levels of MDA and ROS, downregulated the mRNA expressions of TLR4 and MyD88, suppressed the protein levels of p-IκBα and p-p65, and upregulated the protein expression of PPARγ. In summary, licochalcone A protected dairy cow claw dermal cells against LPS-induced inflammatory response and oxidative stress through the regulation of TLR4/MyD88/NF-κB and PPARγ signaling pathways.

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Cistanches alleviates sevoflurane‐induced cognitive dysfunction by regulating PPAR‐γ‐dependent antioxidant and anti‐inflammatory in rats

Cited by 40 publications

References 48 publications

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

A new mechanism of POCD caused by sevoflurane in mice: cognitive impairment induced by cross-dysfunction of iron and glucose metabolism

The protective effect of licochalcone A against inflammation injury of primary dairy cow claw dermal cells induced by lipopolysaccharide

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