The anti-inflamm-aging and hepatoprotective effects of huperzine A in d-galactose-treated rats

Ruan, Qingwei; Liu, Fang; Gao, Zhanjuan; Kong, Dan; Hu, Xiaona; Shi, Dongmei; Bao, Zhijun; Yu, Zhuowei

doi:10.1016/j.mad.2012.12.005

Cited by 53 publications

(41 citation statements)

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“…The liver and the kidney injury model, induced by D-gal treatment (100-500 mg/kg body weight, s.c.) for 8 weeks in mice or rats, has been widely accepted (Fan et al 2009;Ruan et al 2013). The chronic subcutaneous administration of D-gal for 8 weeks induced oxidative stress, hepatopathy, and nephropathy in mice and significantly decreased the hepatic and renal SOD and CAT activities as well as GSH levels, increased the hepatic and renal MDA levels (Fan et al 2009;Yu et al 2015).…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic acid protects d-galactose-induced liver and kidney injury via antioxidation and anti-inflammation effects in mice

Feng

Wang

et al. 2016

Pharmaceutical Biology

113

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Context Oxidative stress and inflammation are implicated in the aging process and its related hepatic and renal function decline. Chlorogenic acid (CGA) is one of the most abundant polyphenol compounds in the human diet. Recently, CGA has shown in vivo and in vitro antioxidant properties. Objective The current study investigates the effects of protective effects of chlorogenic acid (CGA) on D-galactose-induced liver and kidney injury. Materials and methods Hepatic and renal injuries were induced in a mouse model by subcutaneously injection of D-galactose (D-gal; 100 mg/kg) once a day for 8 consecutive weeks and orally administered simultaneously with CGA included in the food (200 mg/kg of diet). The liver and renal functions were examined. Histological analyses of liver and kidney were done by haematoxylin and eosin staining. The oxidative stress markers and pro-inflammatory cytokines in the liver and the kidney were measured. Results CGA significantly reduced the serum aminotransferase, serum creatinine (SCr) and blood urea nitrogen (BUN) levels in D-gal mice (p50.05). CGA also restored superoxide dismutase, catalase, and malondialdehyde levels and decreased glutathione content in the liver and kidney in D-gal mice (p50.05). Improvements in liver and kidney were also noted in histopathological studies. CGA reduced tumour necrosis factor-a (TNF-a) and interleukin-6 (IL-6) protein levels in the liver and kidney in D-gal mice (p50.05). Discussion and conclusion These findings suggest that CGA attenuates D-gal-induced chronic liver and kidney injury and that this protection may be due to its antioxidative and antiinflammatory activities.ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Chlorogenic acid protects d-galactose-induced liver and kidney injury via antioxidation and anti-inflammation effects in mice

Feng

Wang

et al. 2016

Pharmaceutical Biology

113

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“…Huperzine A, a reversible and selective AChEI, is an effective intervention drug used to suppress both innate and adaptive inflammatory responses to ischemic brain injury, Alzheimer's disease and myasthenia gravis [19,32,34,58]. In another study, we found that huperzine A also significantly suppressed D -gal-induced hepatic cell replicative senescence by inhibiting NF-κB-mediated inflammation [10]. One specific biomarker used to characterize the chronic administration of D -gal-induced aging in mice was the marked increase in AChE [6].…”

Section: Discussionmentioning

confidence: 99%

“…AChEIs can induce cholinergic upregulation with subsequent effects on neuroinflammation and hepatic inflammation, such as hepatic and T-cell proliferation, glial activation and cytokine production [10,20,32]. Huperzine A has been widely used to improve cognitive and memory deficits in patients with benign senescent forgetfulness, Alzheimer's disease and vascular dementia via noncholinergic mechanisms, including attenuating oxidative stress, inhibiting apoptosis and interfering with amyloid precursor protein metabolism [33,34,35,36].…”

Section: Introductionmentioning

confidence: 99%

The Neurovascular Protective Effects of Huperzine A on D-Galactose-Induced Inflammatory Damage in the Rat Hippocampus

Ruan

et al. 2014

Gerontology

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Background: Chronic administration of D-galactose (D-gal) results in oxidative stress and chronic inflammatory aging. Age-related changes in the brain result in neurovascular damage and blood-brain barrier (BBB) dysfunction. However, little is known regarding D-gal-induced neurovascular damage, as well as the protective effects of huperzine A. Objective: The purpose of this study was to utilize a D-gal-induced rat model to investigate the activation of neurovascular inflammatory damage and apoptosis in the rat hippocampus and to understand whether huperzine A alleviates D-gal-induced neuronal and vascular inflammatory injury. Methods: Aging rats were treated with D-gal (300 mg/kg s.c. for 8 weeks), were coadministered D-gal and huperzine A (D-gal 300 mg/kg and huperzine A 0.1 mg/kg s.c. for 8 weeks) or served as the saline-treated control group rats (same volume of saline given subcutaneously for 8 weeks). Changes in hippocampal morphology and biomarkers of inflammatory damage were analyzed. Results: Our study revealed that chronic administration of D-gal resulted in the activation of glia and vascular endothelial cells and upregulation of mRNA and protein levels of cell-associated adhesion molecules and inflammatory cytokines via nuclear factor (NF)-κB inhibitor degradation and NF-κB nuclear translocation. The inflammatory injury caused significant BBB dysfunction, decreased density of tight junctions (TJs) and apoptosis in the rat hippocampus. Coadministration of huperzine A not only markedly inhibited the D-gal-induced increase in acetylcholinesterase (AChE) activity, but also alleviated D-gal-induced neurovascular damage by inhibiting D-gal-induced NF-κB activation, improving cerebrovascular function and suppressing the D-gal-induced decrease in the density and protein levels of TJs and cell apoptosis. Conclusions: Our findings provided evidence that D-gal induced a proinflammatory phenotype mediated by NF-κB in the rat hippocampus. Moreover, huperzine A suppressed D-gal-induced neurovascular damage and BBB dysfunction, partly by preventing NF-κB nuclear translocation. The inhibiting effect of huperzine A on AChE activity might play an important role in attenuating D-gal-induced inflammatory damage.

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“…To measure the production of reactive oxygen species (ROS) and malondialdehyde (MDA), ROS generation in the brain was determined in tissue homogenates by using dichlorofluorescein diacetate (DCFH-DA) [20]. The tissue homogenate was incubated with 1 mM 2′,7′-dichlorodihydrofluorescein diacetate for 30 min at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

Effects of pretreatment with methanol extract of Peucedani Radix on transient ischemic brain injury in mice

et al. 2017

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BackgroundStroke is the second most common cause of death and may result in various disabilities; thus, identification of neuroprotective therapeutic agents is important. Peucedani Radix (PR), the root of Angelica decursiva, is a well-known remedy for damp and phlegm in Korean medicine and has also been shown to exert antioxidant and anti-inflammatory activities. This study was performed to investigate the mechanism underlying the anti-inflammatory effect of methanol extract of PR (PRex) on cerebral ischemic injury.MethodsC57BL/6 male mice were orally administered PRex (20, 60, or 200 mg/kg) at 2 days, 1 day, and 1 h prior to middle cerebral artery occlusion (MCAO). Twenty-four hours after MCAO, the infarct volume was measured and the neurological deficit score was assessed. The inflammatory-related substances in the ipsilateral hemisphere were determined by western blotting, DCFH-DA assay, TBARS assay, and ELISA.ResultsPRex pretreatment significantly decreased the infarct volume at 24 h after MCAO. Moreover, PRex effectively suppressed the expression of iNOS, ROS, MDA, and pro-inflammatory cytokines, such as IL-1β and TNF-α, in brain tissue of mice with MCAO-induced brain injury.ConclusionsPRex protected neurons from ischemic brain injury in mice through its antioxidant and anti-inflammatory activities. Our results suggested that PR could be a promising candidate in the therapy of ischemia-induced brain damage.Electronic supplementary materialThe online version of this article (doi:10.1186/s13020-017-0151-z) contains supplementary material, which is available to authorized users.

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The anti-inflamm-aging and hepatoprotective effects of huperzine A in d-galactose-treated rats

Cited by 53 publications

References 50 publications

Chlorogenic acid protects d-galactose-induced liver and kidney injury via antioxidation and anti-inflammation effects in mice

Chlorogenic acid protects d-galactose-induced liver and kidney injury via antioxidation and anti-inflammation effects in mice

The Neurovascular Protective Effects of Huperzine A on D-Galactose-Induced Inflammatory Damage in the Rat Hippocampus

Effects of pretreatment with methanol extract of Peucedani Radix on transient ischemic brain injury in mice

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