Baicalein pretreatment reduces liver ischemia/reperfusion injury via induction of autophagy in rats

Liu, Anding; Huang, Liang; Guo, Enshuang; Li, Renlong; Yang, Jiankun; Li, An-Yi; Yang, Yan; Liu, Shenpei; Hu, Jifa; Jiang, Xiaojing; Dirsch, Olaf; Dahmen, Uta; Sun, Jian

doi:10.1038/srep25042

Cited by 58 publications

(52 citation statements)

References 32 publications

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“…Primary rat hepatocytes were isolated and cultured by a modified in situ collagenase perfusion technique as described (Kim, Qian, & Lemasters, 2003; Liu, Guo, et al., 2016; Liu, Huang, et al., 2016). Briefly, after anesthetizing with pentobarbital, liver was perfused in situ with warm Hank's Balanced Salt Solution (Life Technologies, 14175) via the portal vein and was followed by liver warm basic Dulbecco's Modified Eagle's Medium (DMEM, Life Technologies, 11995) containing 0.75 mg/ml collagenase D (Sigma‐Aldrich, C5138) for 10–15 min.…”

Section: Methodsmentioning

confidence: 99%

Young plasma reverses age‐dependent alterations in hepatic function through the restoration of autophagy

et al. 2017

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SummaryRecent studies showing the therapeutic effect of young blood on aging‐associated deterioration of organs point to young blood as the solution for clinical problems related to old age. Given that defective autophagy has been implicated in aging and aging‐associated organ injuries, this study was designed to determine the effect of young blood on aging‐induced alterations in hepatic function and underlying mechanisms, with a focus on autophagy. Aged rats (22 months) were treated with pooled plasma (1 ml, intravenously) collected from young (3 months) or aged rats three times per week for 4 weeks, and 3‐methyladenine or wortmannin was used to inhibit young blood‐induced autophagy. Aging was associated with elevated levels of alanine transaminase and aspartate aminotransferase, lipofuscin accumulation, steatosis, fibrosis, and defective liver regeneration after partial hepatectomy, which were significantly attenuated by young plasma injections. Young plasma could also restore aging‐impaired autophagy activity. Inhibition of the young plasma‐restored autophagic activity abrogated the beneficial effect of young plasma against hepatic injury with aging. In vitro, young serum could protect old hepatocytes from senescence, and the antisenescence effect of young serum was abrogated by 3‐methyladenine, wortmannin, or small interfering RNA to autophagy‐related protein 7. Collectively, our data indicate that young plasma could ameliorate age‐dependent alterations in hepatic function partially via the restoration of autophagy.

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Section: Methodsmentioning

confidence: 99%

Young plasma reverses age‐dependent alterations in hepatic function through the restoration of autophagy

et al. 2017

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“…Baicalein also has the ability to protect against acute liver failure induced by D-galactosamine/lipopolysaccharides [17]. Recent results have demonstrated that baicalein pretreatment reduces liver ischemia/reperfusion injury via induction of autophagy in rats [35]. Another agent, rutin, which is similar in chemical structure to baicalein, has also shown hepatoprotective activity against biliary obstruction or CCl 4 -induced liver injury [36,37].…”

Section: Resultsmentioning

confidence: 99%

Baicalein and its underlying mechanism as a protector against liver injury induced by cisplatin in mice

Niu

Wan

Bian

et al. 2016

Biotechnology & Biotechnological Equipment

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Cisplatin is widely used for the treatment of a variety of cancers but with a high incidence of hepatotoxicity. Baicalein is originally isolated from the root of Scutellaria baicalensis Georgi with broad bioactivities. The present study aims to investigate the protective effect of baicalein against cisplatin-induced acute liver injury and the underlying mechanism of this protective effect. Administration of cisplatin (40 mg/kg) for 24 h increased the serum alanine and aspartate aminotransferases and alkaline phosphatase levels, while baicalein could reverse all those changes induced by cisplatin. Liver histological analysis further evidenced the protection of baicalein against cisplatin-induced liver injury. Baicalein counteracted the increased liver malondialdehyde (amount induced by cisplatin, while baicalein could further increase the cisplatin-induced elevation of the amount of reduced glutathione in the liver. Further results showed that baicalein reversed the cisplatin-induced decrease in the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S transferase and glutathione reductase. On the other hand, baicalein alleviated the increase in the serum levels of tumour necrosis factor alpha and interleukin 6 induced by cisplatin. Taken together, our results demonstrate that baicalein can inhibit cisplatininduced hepatic oxidative stress and inflammation, which contributes greatly to the amelioration of cisplatin-induced liver injury.

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“…34) Baicalein is able to increase autophagy. 17) It is reported that heme oxygenase-1 (HO-1) is a key mediator of autophagy. 35,36) HO-1, a stress-responsive enzyme, degrades intracellular heme to free iron, carbon monoxide and biliverdin.…”

Section: Discussionmentioning

confidence: 99%

“…39) Baicalein could ameliorate liver I/R injury via induction of HO-1-mediated autophagy. 17) Mitochondrial dysfunction, as well as autophagic impairment is involved in the pathogenesis of PD. Mitochondrial autophagy (or mitophagy), which selectively removes damaged and dysfunctional mitochondria, has been shown to play an important role in maintaining mitochondrial homeostasis and preventing cell death.…”

Section: Discussionmentioning

confidence: 99%

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Baicalein Protects against Rotenone-Induced Neurotoxicity through Induction of Autophagy

Kuang

Cao

2017

Biological & Pharmaceutical Bulletin

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Baicalein, a typical flavonoid compound, has neuroprotective properties in several neurological disorders. Autophagy plays a central role in maintaining the cellular homeostasis, and is involved in the pathogenesis of Parkinson's disease (PD). Recently, baicalein has been reported to induce autophagy. Therefore, the current study was designed to investigate whether baicalein could protect against rotenone-induced neurotoxicity via induction of autophagy both in SH-SY5Y cells and in a mouse model. A chronic PD mouse model was established by continuous intragastric administration of rotenone for 12 weeks. Baicalein was administrated from 7 to 12 week. Our results showed that baicalein prevented rotenone-induced behavioral deficits, dopaminergic neuronal loss, apoptosis and mitochondrial dysfunction. Furthermore, baicalein restored rotenone-impaired autophagy, and blocking the baicalein-induced autophagy using 3-methyladenine inhibited the neuroprotective effects of bacalein. Baicalein increased cell viability and restored mitochondrial function in SH-SY5Y cells. The beneficial effect of baicalein was abrogated by 3-methyladenine treatment. Furthermore, rapamycin increased autopahgy and reduced the rotenone-induced neurotoxicity in SH-SY5Y cells. Collectively, these results suggest that baicalein could prevent rotenone-induced neurotoxicity via restoring autophagy. Key words baicalein; neuroprotection; Parkinson's disease; autophagyParkinson's disease (PD) is a progressive neurodegenerative disorder characterized by bradykinesia, rigidity, resting tremor, and postural instability.1-3) The main pathological characteristic of PD is the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta, the loss of dopamine in the striatum, and the presence of intracytoplasmic inclusions in surviving neurons known as Lewy bodies.4) Several biochemical mechanisms related to the pathogenesis of PD include oxidative stress, mitochondrial dysfunction, protein aggregation and misfolding, apoptosis, excitotoxicity, and neuroinflammation.5,6) Currently, none of therapies has been convincingly shown to slow down or prevent the progression of PD, and additional effective treatments for this disease are urgently needed.Baicalein, a flavonoid, is derived from the root of the traditional Chinese herb Scutellariabaicalensis GEORGI. Baicalein has been reported to have neuroprotective effects in PD model through anti-inflammatory, anti-apoptosis, and anti-oxidative actions. In vitro, baicalein protected PC12 cells against 6-hydroxydopamine (6-OHDA)-or rotenone-induced neurotoxicity, 7,8) and ameliorated the 6-OHDA-induced SH-SY5Y cell apoptosis.9) In vivo, baicalein exerted neuroprotective effects in 6-OHDA-induced neurotoxicity in rats 9) and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in mice.10) However, the exact mechanism of baicalein is poorly understood.Autophagy is a highly conservative cellular process by which cells degrade and recycle of bulk cytosolic proteins and dama...

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Baicalein pretreatment reduces liver ischemia/reperfusion injury via induction of autophagy in rats

Cited by 58 publications

References 32 publications

Young plasma reverses age‐dependent alterations in hepatic function through the restoration of autophagy

Young plasma reverses age‐dependent alterations in hepatic function through the restoration of autophagy

Baicalein and its underlying mechanism as a protector against liver injury induced by cisplatin in mice

Baicalein Protects against Rotenone-Induced Neurotoxicity through Induction of Autophagy

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