Effect of Angelica polysaccharide on brain senescence of Nestin-GFP mice induced by D-galactose

Cheng, Xiuyuan; Yao, Hui; Xiang, Yang; Chen, Linbo; Xiao, Minghe; Wang, Ziling; Xiao, Hanxianzhi; Wang, Lu; Wang, Shunhe; Wang, Yaping

doi:10.1016/j.neuint.2018.09.003

Cited by 46 publications

(33 citation statements)

References 35 publications

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“…25,26 Through decreasing the levels of IL-1β, IL-6, and TNF-a, and enhancing the antioxidant, APS improves neurogenesis and brain senescence in Chen et al . 27 In this study, we found that ASP could significantly reduce the expressions of inflammatory factors in AD rats. Taken together, all of these studies suggested that ASP could ameliorate spatial learning and memory deficiency, and decrease free radical metabolism and neuroinflammation in AD rats.…”

Section: Discussionmentioning

confidence: 55%

Angelica polysaccharide ameliorates memory impairment in Alzheimer’s disease rat through activating BDNF/TrkB/CREB pathway

Zhu

2019

Exp Biol Med (Maywood)

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This study aimed to investigate the effect of Angelica sinensis polysaccharides (ASP) on Alzheimer’s disease (AD) and its underlying mechanisms. In our study, we build the AD model by injecting Aβ25–35. Morris water maze (MWM) was applied to investigate learning and memory. Moreover, neurotransmitters, free radical, and inflammatory factors were also measured. Pathological change and neuronal death in hippocampus CA1, CA3, and DG region were detected by HE staining and Nissl staining. The neuronal apoptosis was detected by TUNEL. The expressions of caspase-3, Bcl-2 and Bax were measured by immunohistochemistry and Western blot. The expressions of BDNF, TrkB, p-Akt, Akt, p-CREB, and CREB were measured by Western blot. Our results showed that ASP could ameliorate spatial learning and memory deficiency in AD rats. ASP decreased AchE level and increased the levels of Ach and chAT in AD rats. ASP could increase the activity of SOD and CAT, decrease MDA activity, and inhibit the expression levels of inflammatory factors and neurons apoptosis in AD rats. Pathological change of hippocampus CA1, CA3, and DG region was ameliorated by ASP. In addition, the effects of ASP were reversed by K252a (TrkB inhibitor). Our study demonstrated that ASP could ameliorate memory impairment in AD rat through activating BDNF/TrkB/CREB pathway. Impact statement The present study demonstrated that ASP could ameliorate memory impairment through regulation of the balance of neurotransmitters, free radical metabolism, inflammation, and neurons apoptosis. Moreover, the mechanism of ASP on memory impairment may be related to BDNF/TrkB/CREB pathway in AD. Our research provides an innovatively regulatory mechanism about the ASP in AD rat and points a new way to the treatment of AD.

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Section: Discussionmentioning

confidence: 55%

Angelica polysaccharide ameliorates memory impairment in Alzheimer’s disease rat through activating BDNF/TrkB/CREB pathway

Zhu

2019

Exp Biol Med (Maywood)

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“…During the inflammatory reaction process, ROS induce the production of inflammatory cytokines. 48 Previously, elevated levels of the pro-inflammatory factors TNF-a, IL-6, 28 and IL-2 27 were linked to radioactive pulmonary fibrosis and other types of pulmonary fibrosis. Recently, there has been little research on the causes of radioactivity-induced salivary gland fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect and Mechanism of Action of Rosmarinic Acid on Radiation-Induced Parotid Gland Injury in Rats

Zhang

Liu

et al. 2020

Dose-Response

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The parotid glands are damaged by oxidative stress and a series of pathophysiological changes after irradiation. Rosmarinic acid (RA) is a natural antioxidant that provides a radioprotective effect against harmful damage from ionizing radiation. The present study aims to explore the protective effects of RA on radiation-induced parotid gland injury and its underlying mechanism. Sprague-Dawley rats were irradiated with 15 Gy X-ray and treated with different concentrations of RA (30, 60, and 120 mg/kg) or amifostine (AMI, 250 mg/kg). Saliva secretion function, oxidative stress, apoptosis, the inflammatory response, and fibrosis were determined by the measurement of the salivary flow rate, enzyme-linked immunosorbent assay, transferase-mediated DUTP Nick end labeling, Western blot, quantitative real time polymerase chain reaction, and hematoxylin and eosin staining. Here, we show that RA treatment significantly attenuated reactive oxygen species by a direct hindrance effect and the indirect activation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha/nicotinamide adenine dinucleotide phosphate oxidase 4 signaling. Rosmarinic acid not only reduced apoptosis by inhibiting p53/jun N-terminal kinase activation but also reduced parotid gland tissue fibrosis by downregulating inflammatory factor levels. Compared to AMI, RA has the obvious advantages of late efficacy and convenient usage. Moreover, 60 mg/kg is the minimum effective dose of RA. Therefore, RA can potentially be applied as a therapeutic radioprotective agent to treat radiation-induced parotid gland injury in the future.

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“…By investigating the effects of ASP, different studies concluded that ASP has the role of protecting NSCs against aging [ 195 , 196 ]. Nestin-green fluorescent protein (GFP) transgenic mouse is a model constructed to explore the antiaging process and be able to detect the number, distribution, differentiation, and migration pathways of NSCs in the brain tissue using fluorescence-labeled nestin.…”

Section: Herb-derived Products With An Antiaging and Antisenescentmentioning

confidence: 99%

“…In fact, owing to ASP treatment, cell proliferation increased in a dose-dependent manner, the levels of both MDA and ROS were reduced, and conversely, the activity of SOD and T-AOC resulted to be increased. Finally, inflammatory cytokines (IL-1 β , IL-6, and TNF- α ) were also reduced and the cellular senescence-associated genes p53 and p21 were downregulated [ 196 ].…”

Section: Herb-derived Products With An Antiaging and Antisenescentmentioning

confidence: 99%

Herb-Derived Products: Natural Tools to Delay and Counteract Stem Cell Senescence

Abruzzo

Canaider

Pizzuti

et al. 2020

Stem Cells International

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Cellular senescence plays a very important role in organismal aging increasing with age and in age-related diseases (ARDs). This process involves physiological, structural, biochemical, and molecular changes of cells, leading to a characteristic trait referred to “senescence-associated secretory phenotype (SASP).” In particular, with aging, stem cells (SCs) in situ exhibit a diminished capacity of self-renewal and show a decline in their functionality. The identification of interventions able to prevent the accumulation of senescent SCs in the organism or to pretreat cultured multipotent mesenchymal stromal cells (MSCs) prior to employing them for cell therapy is a main purpose of medical research. Many approaches have been investigated and resulted effective to prevent or counteract SC senescence in humans, as well as other animal models. In this work, we have reviewed the chance of using a number of herb-derived products as novel tools in the treatment of cell senescence, highlighting the efficacy of these agents, often still far from being clearly understood.

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Effect of Angelica polysaccharide on brain senescence of Nestin-GFP mice induced by D-galactose

Cited by 46 publications

References 35 publications

Angelica polysaccharide ameliorates memory impairment in Alzheimer’s disease rat through activating BDNF/TrkB/CREB pathway

Angelica polysaccharide ameliorates memory impairment in Alzheimer’s disease rat through activating BDNF/TrkB/CREB pathway

Protective Effect and Mechanism of Action of Rosmarinic Acid on Radiation-Induced Parotid Gland Injury in Rats

Herb-Derived Products: Natural Tools to Delay and Counteract Stem Cell Senescence

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