Huperzine A (HupA), extracted from a club moss (Huperzia serrata), is a
sesquiterpene alkaloid and a powerful and reversible inhibitor of
acetylcholinesterase (AChE) with on- and off-rates. [6,8] Huperzia has been used in
China for centuries for the treatment of swelling, fever and blood disorders. It has
demonstrated both memory enhancement in animal and clinical trials and
neuroprotective effects. [5]
Pharmacokinetics
Compared with tacrine, donepezil, and rivastigmine, HupA has better penetration
through the blood-brain barrier, higher oral bioavailability, and longer duration of
acetylcholinesterase inhibitory action. [1]
Pharmacokinetic studies in rodents, canines, and healthy human volunteers
indicated that Huperzine A was absorbed rapidly, distributed widely in the body, and
eliminated at a moderate rate with the property of slow and prolonged release after
oral administration. [1]
Pharmacology
Huperzine A has been found to have benefits of reversing or attenuating cognitive
deficits in a broad range of animal models. Clinical trials have demonstrated that
Huperzine A relieves memory deficits in aged subjects, patients with benign
senescent forgetfulness, Alzheimer's disease and vascular dementia, with minimal
peripheral cholinergic side effects compared with other AChEIs in use. [2]
Huperzine A possesses the benefits or ability to protect cells against hydrogen
peroxide, beta-amyloid protein (or peptide), glutamate, ischemia and
staurosporine-induced cytotoxicity and apoptosis. These protective effects are
related to its ability to attenuate oxidative stress, regulate the expression of
apoptotic proteins Bcl-2, Bax, P53 and caspase-3, protect mitochondria, and
interfere with APP metabolism. Antagonizing effects on NMDA receptors and
potassium currents may contribute to the neuroprotection as well. It is also possible
that the non-catalytic function of AChE is involved in neuroprotective effects of
Huperzine A. The therapeutic effects of Huperzine A on Alzheimer's disease or
vascular dementia are probably exerted via a multi-target mechanism. [2]
Studies about its beneficial claims:
In-vitro Studies
Researchers found that huperzine A protects neurons against Abeta25-35-induced
apoptosis via the inhibition of ROS formation and caspase-3 activity. In the
experiment, huperzine A reduced Abeta25-35-induced ROS formation in a
dose-dependent manner. [10]
Treatment of PC12 cells with 10 micromol/L Huperzine A for 48 h markedly
increased the number of neurite-bearing cells, but caused no significant alteration in
cell viability or other signs of cytotoxicity. In addition to inhibiting AChE activity, 10
micromol/L Huperzine A also increased the mRNA and protein levels of this enzyme.
In addition, following 2 h exposure of the astrocytes to 10 micromol/L Huperzine A,
there was a significant up-regulation of mRNA for NGF and P75 low-affinity NGF
receptor. The protein level of NGF was also increased after 24 h treatment with
Huperzine A. Thus, these findings demonstrate that Huperzine has an neurotrophic
activity, which might be beneficial in treatment of neurodegenerative disorders such
as Alzheimer disease. [3]
Animal Studies
L-Huperzine-A was administered systemically or locally through the microdialysis
probe into the rat cortex. In both cases, acetylcholine, norepinephrine and dopamine
levels were increased significantly. Thus, L-Huperzine-A is a potent inhibitor of
cholinesterase which penetrates into the brain and produces a dose-dependent
increase of acetylcholine, morepinephrine, and dopamine in rat cortex. [7]
Huperzine A has been shown in animal studies that it can be used as a protective
agent against organophosphate (OP) intoxication and that it reduces
glutamate-induced cell death. [5]
Clinical Studies
Huperzine A has undergone double-blind, placebo-controlled clinical trials in
patients with Alzheimer's disease (AD), with significant improvements both to
cognitive function and the quality of life. [5]
The therapeutic effects of Huperzine A were studied by random, match and
double-blind method on 56 patients of multi-infarct dementia or senile dementia and
104 patients of senile and presenile simple memory disorders. The im dose for
multi-infarct dementia was 0.05 mg bid for 4 wk, whereas that for senile and
presenile simple memory disorders was 0.03 mg bid for 2 wk. Saline was used on
control group. The result showed that the curative effect of huperzine A was
significant. [4]
Safety and Side Effects of Huperzine A
Animal and clinical safety tests showed that Huperzine A had no unexpected toxicity,
particularly the dose-limiting hepatotoxicity induced by tacrine. The phase IV clinical
trials in China have demonstrated that Huperzine A significantly improved memory
deficits in elderly people with benign senescent forgetfulness, and patients with
Alzheimer disease and vascular dementia, with minimal peripheral cholinergic side
effects and no unexpected toxicity. Huperzine A can also be used as a protective
agent against organophosphate intoxication. [1,5]
Medications that prevent acetylcholine breakdown often produce side effects,
including nausea, vomiting, excess saliva and tear production, and sweating. In a
study of 56 patients suffered from dementia, a few patients felt slight dizziness. [4]
Reference
SOURCE [1] Wang R, et al, Progress in studies of huperzine A, a natural
cholinesterase inhibitor from Chinese herbal medicine. Acta Pharmacol Sin. 2006
Jan;27(1):1-26. [2] Wang R, Neuroprotective effects of huperzine A. A natural
cholinesterase inhibitor for the treatment of Alzheimer's disease. Neurosignals.
2005;14(1-2):71-82. [3] Tang LL, Wang R, Tang XC. Effects of huperzine A on
secretion of nerve growth factor in cultured rat cortical astrocytes and neurite
outgrowth in rat PC12 cells. Acta Pharmacol Sin. 2005 Jun;26(6):673-8. [4] Zhang
RW, et al, Drug evaluation of huperzine A in the treatment of senile memory
disordersZhongguo Yao Li Xue Bao. 1991 May;12(3):250-2. [5] Zangara A. The
psychopharmacology of huperzine A: an alkaloid with cognitive enhancing and
neuroprotective properties of interest in the treatment of Alzheimer's disease.
Pharmacol Biochem Behav. 2003 Jun;75(3):675-86. [6] Ashani Y, Peggins JO 3rd,
Doctor BP. Mechanism of inhibition of cholinesterases by huperzine A. Biochem
Biophys Res Commun. 1992 Apr 30;184(2):719-26. [7] Zhu XD, Giacobini E. Second
generation cholinesterase inhibitors: effect of (L)-huperzine-A on cortical biogenic
amines. J Neurosci Res. 1995 Aug 15;41(6):828-35. [8] Tang XC. Huperzine A
(shuangyiping): a promising drug for Alzheimer's disease. Zhongguo Yao Li Xue
Bao. 1996 Nov;17(6):481-4. [9] Patocka J. Huperzine A--an interesting
anticholinesterase compound from the Chinese herbal medicine. Acta Medica
(Hradec Kralove). 1998;41(4):155-7. [10] Xiao XQ, Zhang HY, Tang XC. Huperzine A
attenuates amyloid beta-peptide fragment 25-35-induced apoptosis in rat cortical
neurons via inhibiting reactive oxygen species formation and caspase-3 activation. J
Neurosci Res. 2002 Jan 1;67(1):30-6.
sesquiterpene alkaloid and a powerful and reversible inhibitor of
acetylcholinesterase (AChE) with on- and off-rates. [6,8] Huperzia has been used in
China for centuries for the treatment of swelling, fever and blood disorders. It has
demonstrated both memory enhancement in animal and clinical trials and
neuroprotective effects. [5]
Pharmacokinetics
Compared with tacrine, donepezil, and rivastigmine, HupA has better penetration
through the blood-brain barrier, higher oral bioavailability, and longer duration of
acetylcholinesterase inhibitory action. [1]
Pharmacokinetic studies in rodents, canines, and healthy human volunteers
indicated that Huperzine A was absorbed rapidly, distributed widely in the body, and
eliminated at a moderate rate with the property of slow and prolonged release after
oral administration. [1]
Pharmacology
Huperzine A has been found to have benefits of reversing or attenuating cognitive
deficits in a broad range of animal models. Clinical trials have demonstrated that
Huperzine A relieves memory deficits in aged subjects, patients with benign
senescent forgetfulness, Alzheimer's disease and vascular dementia, with minimal
peripheral cholinergic side effects compared with other AChEIs in use. [2]
Huperzine A possesses the benefits or ability to protect cells against hydrogen
peroxide, beta-amyloid protein (or peptide), glutamate, ischemia and
staurosporine-induced cytotoxicity and apoptosis. These protective effects are
related to its ability to attenuate oxidative stress, regulate the expression of
apoptotic proteins Bcl-2, Bax, P53 and caspase-3, protect mitochondria, and
interfere with APP metabolism. Antagonizing effects on NMDA receptors and
potassium currents may contribute to the neuroprotection as well. It is also possible
that the non-catalytic function of AChE is involved in neuroprotective effects of
Huperzine A. The therapeutic effects of Huperzine A on Alzheimer's disease or
vascular dementia are probably exerted via a multi-target mechanism. [2]
Studies about its beneficial claims:
In-vitro Studies
Researchers found that huperzine A protects neurons against Abeta25-35-induced
apoptosis via the inhibition of ROS formation and caspase-3 activity. In the
experiment, huperzine A reduced Abeta25-35-induced ROS formation in a
dose-dependent manner. [10]
Treatment of PC12 cells with 10 micromol/L Huperzine A for 48 h markedly
increased the number of neurite-bearing cells, but caused no significant alteration in
cell viability or other signs of cytotoxicity. In addition to inhibiting AChE activity, 10
micromol/L Huperzine A also increased the mRNA and protein levels of this enzyme.
In addition, following 2 h exposure of the astrocytes to 10 micromol/L Huperzine A,
there was a significant up-regulation of mRNA for NGF and P75 low-affinity NGF
receptor. The protein level of NGF was also increased after 24 h treatment with
Huperzine A. Thus, these findings demonstrate that Huperzine has an neurotrophic
activity, which might be beneficial in treatment of neurodegenerative disorders such
as Alzheimer disease. [3]
Animal Studies
L-Huperzine-A was administered systemically or locally through the microdialysis
probe into the rat cortex. In both cases, acetylcholine, norepinephrine and dopamine
levels were increased significantly. Thus, L-Huperzine-A is a potent inhibitor of
cholinesterase which penetrates into the brain and produces a dose-dependent
increase of acetylcholine, morepinephrine, and dopamine in rat cortex. [7]
Huperzine A has been shown in animal studies that it can be used as a protective
agent against organophosphate (OP) intoxication and that it reduces
glutamate-induced cell death. [5]
Clinical Studies
Huperzine A has undergone double-blind, placebo-controlled clinical trials in
patients with Alzheimer's disease (AD), with significant improvements both to
cognitive function and the quality of life. [5]
The therapeutic effects of Huperzine A were studied by random, match and
double-blind method on 56 patients of multi-infarct dementia or senile dementia and
104 patients of senile and presenile simple memory disorders. The im dose for
multi-infarct dementia was 0.05 mg bid for 4 wk, whereas that for senile and
presenile simple memory disorders was 0.03 mg bid for 2 wk. Saline was used on
control group. The result showed that the curative effect of huperzine A was
significant. [4]
Safety and Side Effects of Huperzine A
Animal and clinical safety tests showed that Huperzine A had no unexpected toxicity,
particularly the dose-limiting hepatotoxicity induced by tacrine. The phase IV clinical
trials in China have demonstrated that Huperzine A significantly improved memory
deficits in elderly people with benign senescent forgetfulness, and patients with
Alzheimer disease and vascular dementia, with minimal peripheral cholinergic side
effects and no unexpected toxicity. Huperzine A can also be used as a protective
agent against organophosphate intoxication. [1,5]
Medications that prevent acetylcholine breakdown often produce side effects,
including nausea, vomiting, excess saliva and tear production, and sweating. In a
study of 56 patients suffered from dementia, a few patients felt slight dizziness. [4]
Reference
SOURCE [1] Wang R, et al, Progress in studies of huperzine A, a natural
cholinesterase inhibitor from Chinese herbal medicine. Acta Pharmacol Sin. 2006
Jan;27(1):1-26. [2] Wang R, Neuroprotective effects of huperzine A. A natural
cholinesterase inhibitor for the treatment of Alzheimer's disease. Neurosignals.
2005;14(1-2):71-82. [3] Tang LL, Wang R, Tang XC. Effects of huperzine A on
secretion of nerve growth factor in cultured rat cortical astrocytes and neurite
outgrowth in rat PC12 cells. Acta Pharmacol Sin. 2005 Jun;26(6):673-8. [4] Zhang
RW, et al, Drug evaluation of huperzine A in the treatment of senile memory
disordersZhongguo Yao Li Xue Bao. 1991 May;12(3):250-2. [5] Zangara A. The
psychopharmacology of huperzine A: an alkaloid with cognitive enhancing and
neuroprotective properties of interest in the treatment of Alzheimer's disease.
Pharmacol Biochem Behav. 2003 Jun;75(3):675-86. [6] Ashani Y, Peggins JO 3rd,
Doctor BP. Mechanism of inhibition of cholinesterases by huperzine A. Biochem
Biophys Res Commun. 1992 Apr 30;184(2):719-26. [7] Zhu XD, Giacobini E. Second
generation cholinesterase inhibitors: effect of (L)-huperzine-A on cortical biogenic
amines. J Neurosci Res. 1995 Aug 15;41(6):828-35. [8] Tang XC. Huperzine A
(shuangyiping): a promising drug for Alzheimer's disease. Zhongguo Yao Li Xue
Bao. 1996 Nov;17(6):481-4. [9] Patocka J. Huperzine A--an interesting
anticholinesterase compound from the Chinese herbal medicine. Acta Medica
(Hradec Kralove). 1998;41(4):155-7. [10] Xiao XQ, Zhang HY, Tang XC. Huperzine A
attenuates amyloid beta-peptide fragment 25-35-induced apoptosis in rat cortical
neurons via inhibiting reactive oxygen species formation and caspase-3 activation. J
Neurosci Res. 2002 Jan 1;67(1):30-6.
HEALTH BENEFITS OF HUPERZINE A AND ITS SIDE EFFECTS
Huperzia serrata; Herba Huperziae serratae she zu shi shan 蛇足石杉,qian ceng ta,千層塔,Huperszine ARelated
Names: She zu shi shan, 蛇 足 石 杉 ,qian ceng ta 千 層 塔 , jin bu huan, 金不換, qi cun jin 七寸金, qian jin cao 千金草,
she jiao cao 蛇腳草, qian ceng ye, 千層葉, ai song 矮松, shan zhi cao 山芝草, chang bing qian ceng ta, 長柄千層塔
Huperzia serrata; Herba Huperziae serratae she zu shi shan 蛇足石杉,qian ceng ta,千層塔,Huperszine ARelated
Names: She zu shi shan, 蛇 足 石 杉 ,qian ceng ta 千 層 塔 , jin bu huan, 金不換, qi cun jin 七寸金, qian jin cao 千金草,
she jiao cao 蛇腳草, qian ceng ye, 千層葉, ai song 矮松, shan zhi cao 山芝草, chang bing qian ceng ta, 長柄千層塔
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Acidophilus
Almond
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Bilberry
Chromium
CLA
Cod Liver Oil
Coenzyme Q
Colostrum
Dandelion
EGCG
Echinacea
Eleuthero
Ellagic Acid
Eve. Primrose Oil
Fish Oil
Flaxseed
Garlic
Ginger
Ginseng
Ginkgo Biloba
Glucosamine
Gotu Kola
Guar Gum
Hyaluronic acid
Lecithin
Lycopene
Milk Thistle
Nattokinase
Passion Flower
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Polycosanol
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Resveratrol
Rhodiola
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Stevia
Whey
Xylitol
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Discuss with your doctor before taking any alternative medicine. This article is for
reference only, it is not a medical advice. All rights reserved. Do not copy this article to
other website or blog.
reference only, it is not a medical advice. All rights reserved. Do not copy this article to
other website or blog.
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