panax ginseng/atrofia

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Protective effects of ginseng saponins on 3-nitropropionic acid-induced striatal degeneration in rats.

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The precise cause of neuronal cell death in Huntington's disease (HD) is not known. Systemic administration of 3-nitropropionic acid (3-NP), an irreversible succinate dehydrogenase inhibitor, not only induces a cellular ATP depletions but also causes a selective striatal degeneration similar to that

[Protective effect of RenShen compound and DanHuang compound on muscle atrophy in suspended rats].

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OBJECTIVE To study the protective effect of RenShen compound and DanHuang compound on muscle atrophy caused by simulated weightlessness in rats. METHODS Percentage and cross sectional area of fibers and ultrastructure of soleus (SOL) and gastrocnemius (GAS) were determined in 30 d tail suspended

Active components from Siberian ginseng (Eleutherococcus senticosus) for protection of amyloid β(25-35)-induced neuritic atrophy in cultured rat cortical neurons.

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Not only neuronal death but also neuritic atrophy and synaptic loss underlie the pathogenesis of Alzheimer's disease as direct causes of the memory deficit. Extracts of Siberian ginseng (the rhizome of Eleutherococcus senticosus) were shown to have protective effects on the regeneration of neurites

Panax ginseng Total Protein Facilitates Recovery from Dexamethasone-Induced Muscle Atrophy through the Activation of Glucose Consumption in C2C12 Myotubes.

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The clinical anti-inflammatory drug dexamethasone (DEX) can cause many side effects such as muscle atrophy for long-term use. Muscle atrophy induced by DEX may be caused by decrease of glucose consumption. Panax ginseng C.A. Meyer was previously considered to be an antiatrophic agent

Preventive Effects of Ginseng Total Saponins on Chronic Corticosterone-Induced Impairment in Astrocyte Structural Plasticity and Hippocampal Atrophy.

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To further explore the underlying antidepressant mechanism of ginseng total saponins (GTS), this study observed the effects on hippocampal astrocyte structural plasticity and hippocampal volume in the corticosterone-induced mouse depression model. Corticosterone (20 mg/kg/day) was administered

[Study of the saponin of Panax ginseng C.A. Meyer. I. Inhibitory effect on adrenal atrophy, thymus atrophy and the decrease of serum K+ concentration induced by cortisone acetate in unilateral adrenalectomized rats (author's transl)].

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Pseudoginsenoside-F11 improves long-term neurological function and promotes neurogenesis after transient cerebral ischemia in mice.

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Stroke is the leading cause of long-term motor disability and cognitive impairment beside the acute brain injury. Recently, neurogenesis has become an attractive strategy for the chronic recovery of stroke. Our previous study showed that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin,

[The preventive effect of total saponins of Panax japonicus on nonsteroidal anti-inflammatory drug-induced enteropathy].

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Objective To investigate the preventive effect of total saponins of Panax japonicus (SPJ) on nonsteroidal anti-inflammatory drug (NSAID)-induced intestinal injuries in mice. Methods NSAID-induced intestinal mucosal damaged models were established by intragastric administration of 5 mg/mL diclofenac

First Report of Tomato yellow leaf curl China virus with Betasatellite Infecting Panax notoginseng.

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Panax notoginseng, an important medicinal herb commonly known as notoginseng, san qi, or tian qi, is in the family Araliaceae. The herb is mainly cultivated in Guangxi and Yunnan provinces of southern China for its root, which is used in Chinese herbal medicine to treat various blood disorders. In

[Cloning and characterization of cDNA encoding Psammosilene tunicoides squalene synthase].

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The total triterpene saponins of Psammosilene tunicoides have significant pharmacologic activity. Psammosilene tunicoides squalene synthase (PSS) is a gateway enzyme to regulate the biosynthesis of total triterpene saponins extracted from the root of Psammosilene tunicoides which is an endangered

Effects of hepatocyte growth-promoting factor and panax notoginseng saponins on intrasplenic hepatocellular autotransplantation.

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OBJECTIVE To increase the weight of liver tissue mass present in spleen and to shorten the regeneration period of transplanted hepatocytes by stimulating DNA synthesis and protection against ischemic-reperfusion injury. METHODS Hepatocyte growth-promoting factor (PHGF) and panax notoginseng saponins

[Protective effect of panax notoginseng saponins against femoral fracture-induced apoptosis in the superficial cells of rat renal cortex].

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OBJECTIVE To study the protective effect of panax notoginseng saponins (PNS) against apoptosis of the superficial cells of rat renal cortex following femoral fracture in rats. METHODS Ninety Wistar rats were randomized into 3 groups, namely the fracture group (n=36), fracture with PNS treatment

[Study on the mechanism of action of total saponins of Panax notoginseng in ameliorating oxidative stress and insulin resistance in rats fed with high fat diet].

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OBJECTIVE To investigate whether total saponins of Panax notoginseng (tPNS) can ameliorate oxidative stress and insulin resistance (IR) in the high fat induced nonalcoholic fatty liver disease (NAFLD) rat model and to explore the relationship between oxidative stress and IR. METHODS Totally 50

Resource investigation of traditional medicinal plant Panax japonicus (T.Nees) C.A. Mey and its varieties in China.

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BACKGROUND Panax japonicus, the perennial herb in the Araliaceae family, was used as the natural medicinal herb by Chinese traditional doctors for more than thousand years. Its rhizome was mainly used as a tonic, anti-inflammatory and hemostatic agent in China. Most of the therapeutic effects of P.

Protective effect of panaxydol against repeated administration of aristolochic acid on renal function and lipid peroxidation products via activating Keap1-Nrf2/ARE pathway in rat kidney

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Panaxydol (PX), a polyacetylenic compound isolated from the roots of Panax notoginseng, is found to possess various biological functions. However, its protective effects against aristolochic acid (AA)-induced renal injury have not been elucidated yet. The present study was undertaken to elucidate

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