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panax notoginseng/atrophy

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文章临床试验专利权
页 1 从 71 结果
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
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
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
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
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
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,
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
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
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
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
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
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
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.
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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