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1
Neuroprotective effect of Salvianolic acid B on an Aβ25-35
peptide-induced mouse Alzheimer’s disease
Presented by
MOHANLAL
M. PHARM(MNP) 1st Year
15PHM2007
mohanlalchoudhary1992@gmail.com
Guided by
Prof. A. R. JUVEKAR
( Professor in Pharmacy)
Institute of Chemical Technology, Matunga
Critical review on research paper
TITLE – Neuroprotective activity of salvianolic acid B on an Aβ25-35
peptide induce mouse model of Alzheimer disease.
Authors - Young Woo Lee , Dong Hyun Kim , Su Jin Jeon , Se Jin Park ,
Jong Min Kim , Jun Man Jung , Hyung Eun Lee , Shin Gil Bae , Hee
Kyong Oh , Kun Ho Ho Son , Jong Hoon Ryu
Journal name – European journal of pharmacology - 704
Impact factor of journal – 2.532
Year – Feb. 2013
Page no. – 70 - 77
Citation – 27
Publication – ELSVIER Publication abd Published by korean univercity
in Science direct database
2
Description
 Alzheimer's is a type of dementia (progressive and irreversible
neurodegenerative disorder in brain) that causes problems with memory,
thinking and behavior.
 The main potential factors that cause Alzheimer disease, are neurofibrillary
tangle (hyperphosphorylated tau proteins) and senile plaques (composed of
amyloid β proteins)
 In Alzheimer disease activation of microglia and astrocytes, increase
inflammatory cytokinine, induce nitric oxide synthase, cox-2, thiobarbituric
acid reactive substance and some neurotransmitter (specially Ach by inhibiting
degredative enzyme) level in brain and blood.
 Salvianolic acid B (SalB) is a polyphenolic compound obtain from the extract
from root of Chinese herbs of Salvia miltiorrhiza (labiatae)
3
method according to the research paper
4
• Animals are purchased and put into
laboratory and subject to feed food and
water ad libitum and kept for 12hr.
light/dark cycle at constant temperature
and humidity.
• ICR Male Mice were anesthetized by the
mixture of Nitrous oxide and oxygen
containing 2% isoflurane.
• Aβ25-35 peptide was dissolved into sterile
saline water, seal and incubated for 4 days
at 37oc to induce peptide aggregation.
• The aggregated peptide is injected in brain
by i.c.v. injection (9 nmol/3µl) into the right
ventricle at 1μl/min but the sham group
are not injected by peptides act as nagitive
control.
 Alzheimer disease are induced after the administration of
aggregated peptide shows the impairment in memory
functions, behaviour and learning.
 These mice are treated with the salvianolic acid B (0 ,1, 3,
and 10 mg/kg/day, p.o.) for 7 days subsequvently.
 After the sub-chronic treatement of salvianolic acid B, the
mice shows significantly improve in memory and learning
behavior on 10mg/kg/day administration.
Evalution :- neuroprotective activity evaluation in mice are
done by passive avoidance test in-vivo in mice.
Western blot analysis , lipid peroxidation and immuno -
histochemistry analysis in isolated hyppocampal tissue of
brain.
Statistics analysis also evalute by one way analysis of
variance.
5
Significance of Area of Research
 Salvianolic acid B has the activity of anti-inflammatory and
anti-oxidant. The major cause of many disease like Alzheimer,
parkinson, diabetes and other stress and infflamatory disorders
in the human are due to infflamation and stress, so the drugs
has potential targets in the novel treatment of these disease.
 Novel target for treatment of Alzheimer’s disease and other
related disorder by modifying the basic moiety of Salvia
miltiorrhiza and also used in combination with other drug.
 These study can significantly improve the inhancement of
memory and learning on treatment of SalB (10mg/kg) in
neurodegenrative disorders.
6
The Author’s work found to be Novel and some of common, but major work is
done by following four references:
 Durairajan, S.S., Yuan,Q., Xie,L., Chan,W.S., Kum,W.F., Koo,I. ,Liu,C.,
Song,Y., Huang, J.D., Klein,W.L.,Li,M. “Salvianolic acid B inhibits Ab
fibril formation and disaggregates preformed fibrils and protects against
Ab-induced cytotoxicty” Neurochem.Int. 2008; 52; 741–750.
 Butterfield, D.A., Boyd-Kimball, D., “Amyloid b-peptide(1-42) contributes
to the oxidative stress and neurodegeneration found in Alzheimer disease
brain” Brain Pathol; 2004; 14; 426–432.
 Du, G.H., Qiu, Y., Zhang, J.T., “Salvianolic acid B protects the memory
functions against transient cerebral ischemia in mice” J. Asian. Nat. Prod.
Res. 2; 2000; 145–152.
 Wang, S.X., Hu, L.M., Gao, X.M., Guo, H., Fan, G.W. “Anti-inflammatory
activity of salvianolic acid B in microglia contributes to its neuroprotective
effect” Neurochem. Res. 35; 2010; 1029–1037.
7
Originality
 Technically this report is correct but some minor
correction are present.
1. The schedule for experiment protocol was not given
properly into this paper.(Stepanichev et al 2005).
2. Number of animals in each experimental groups and
number of groups are not mention clearly.
3. Both Negative and positive error bar are not mention in the
bar graph.
 Almost all the studies are justified.
 Every part of the work has been supported by proper
justification.
 The all the work discussed very well.
8
Technical Correctness
 According to the review article of Zhang et al, 2014 the
passive avoidance task is less significant to test
behavioral study.
 The comparition of the passive avoidance task to the radial
arm water maze task, radial arm maze are more
significant to test the memory and learning behaviour.
 In graphs the results of 1mg/kg and 3mg/kg are not
mention
9
Technical Correctness
Bibliography
 The paper is published in ‘European Journal of Pharmacology
,Neuropharmacology and analgesia for Alzheimer’s diseases, feb-
2013,vol-704.The citation are accurate and refer to the content in
the manuscript which have been produced by citated articles.The 15
references are mentioned.The references have been written in the
priscribed format and is kept uniform as per the guidelines of journal.
10
Illustrations and graphs
11
Fig . 2. The effect of sub-chronic SalB treatment on Aβ25-35 peptide
mediated glial cells activation
12

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1029-Danh muc Sach Giao Khoa khoi 6.pdf
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CRITICAL REVIEW PRESENTATION

  • 1. 1 Neuroprotective effect of Salvianolic acid B on an Aβ25-35 peptide-induced mouse Alzheimer’s disease Presented by MOHANLAL M. PHARM(MNP) 1st Year 15PHM2007 mohanlalchoudhary1992@gmail.com Guided by Prof. A. R. JUVEKAR ( Professor in Pharmacy) Institute of Chemical Technology, Matunga Critical review on research paper
  • 2. TITLE – Neuroprotective activity of salvianolic acid B on an Aβ25-35 peptide induce mouse model of Alzheimer disease. Authors - Young Woo Lee , Dong Hyun Kim , Su Jin Jeon , Se Jin Park , Jong Min Kim , Jun Man Jung , Hyung Eun Lee , Shin Gil Bae , Hee Kyong Oh , Kun Ho Ho Son , Jong Hoon Ryu Journal name – European journal of pharmacology - 704 Impact factor of journal – 2.532 Year – Feb. 2013 Page no. – 70 - 77 Citation – 27 Publication – ELSVIER Publication abd Published by korean univercity in Science direct database 2
  • 3. Description  Alzheimer's is a type of dementia (progressive and irreversible neurodegenerative disorder in brain) that causes problems with memory, thinking and behavior.  The main potential factors that cause Alzheimer disease, are neurofibrillary tangle (hyperphosphorylated tau proteins) and senile plaques (composed of amyloid β proteins)  In Alzheimer disease activation of microglia and astrocytes, increase inflammatory cytokinine, induce nitric oxide synthase, cox-2, thiobarbituric acid reactive substance and some neurotransmitter (specially Ach by inhibiting degredative enzyme) level in brain and blood.  Salvianolic acid B (SalB) is a polyphenolic compound obtain from the extract from root of Chinese herbs of Salvia miltiorrhiza (labiatae) 3
  • 4. method according to the research paper 4 • Animals are purchased and put into laboratory and subject to feed food and water ad libitum and kept for 12hr. light/dark cycle at constant temperature and humidity. • ICR Male Mice were anesthetized by the mixture of Nitrous oxide and oxygen containing 2% isoflurane. • Aβ25-35 peptide was dissolved into sterile saline water, seal and incubated for 4 days at 37oc to induce peptide aggregation. • The aggregated peptide is injected in brain by i.c.v. injection (9 nmol/3µl) into the right ventricle at 1μl/min but the sham group are not injected by peptides act as nagitive control.
  • 5.  Alzheimer disease are induced after the administration of aggregated peptide shows the impairment in memory functions, behaviour and learning.  These mice are treated with the salvianolic acid B (0 ,1, 3, and 10 mg/kg/day, p.o.) for 7 days subsequvently.  After the sub-chronic treatement of salvianolic acid B, the mice shows significantly improve in memory and learning behavior on 10mg/kg/day administration. Evalution :- neuroprotective activity evaluation in mice are done by passive avoidance test in-vivo in mice. Western blot analysis , lipid peroxidation and immuno - histochemistry analysis in isolated hyppocampal tissue of brain. Statistics analysis also evalute by one way analysis of variance. 5
  • 6. Significance of Area of Research  Salvianolic acid B has the activity of anti-inflammatory and anti-oxidant. The major cause of many disease like Alzheimer, parkinson, diabetes and other stress and infflamatory disorders in the human are due to infflamation and stress, so the drugs has potential targets in the novel treatment of these disease.  Novel target for treatment of Alzheimer’s disease and other related disorder by modifying the basic moiety of Salvia miltiorrhiza and also used in combination with other drug.  These study can significantly improve the inhancement of memory and learning on treatment of SalB (10mg/kg) in neurodegenrative disorders. 6
  • 7. The Author’s work found to be Novel and some of common, but major work is done by following four references:  Durairajan, S.S., Yuan,Q., Xie,L., Chan,W.S., Kum,W.F., Koo,I. ,Liu,C., Song,Y., Huang, J.D., Klein,W.L.,Li,M. “Salvianolic acid B inhibits Ab fibril formation and disaggregates preformed fibrils and protects against Ab-induced cytotoxicty” Neurochem.Int. 2008; 52; 741–750.  Butterfield, D.A., Boyd-Kimball, D., “Amyloid b-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain” Brain Pathol; 2004; 14; 426–432.  Du, G.H., Qiu, Y., Zhang, J.T., “Salvianolic acid B protects the memory functions against transient cerebral ischemia in mice” J. Asian. Nat. Prod. Res. 2; 2000; 145–152.  Wang, S.X., Hu, L.M., Gao, X.M., Guo, H., Fan, G.W. “Anti-inflammatory activity of salvianolic acid B in microglia contributes to its neuroprotective effect” Neurochem. Res. 35; 2010; 1029–1037. 7 Originality
  • 8.  Technically this report is correct but some minor correction are present. 1. The schedule for experiment protocol was not given properly into this paper.(Stepanichev et al 2005). 2. Number of animals in each experimental groups and number of groups are not mention clearly. 3. Both Negative and positive error bar are not mention in the bar graph.  Almost all the studies are justified.  Every part of the work has been supported by proper justification.  The all the work discussed very well. 8 Technical Correctness
  • 9.  According to the review article of Zhang et al, 2014 the passive avoidance task is less significant to test behavioral study.  The comparition of the passive avoidance task to the radial arm water maze task, radial arm maze are more significant to test the memory and learning behaviour.  In graphs the results of 1mg/kg and 3mg/kg are not mention 9 Technical Correctness
  • 10. Bibliography  The paper is published in ‘European Journal of Pharmacology ,Neuropharmacology and analgesia for Alzheimer’s diseases, feb- 2013,vol-704.The citation are accurate and refer to the content in the manuscript which have been produced by citated articles.The 15 references are mentioned.The references have been written in the priscribed format and is kept uniform as per the guidelines of journal. 10
  • 11. Illustrations and graphs 11 Fig . 2. The effect of sub-chronic SalB treatment on Aβ25-35 peptide mediated glial cells activation
  • 12. 12