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Heme oxygenase effect on mesenchymal stem cells action on experimental Alzheimer's disease.

Abdel Aziza MT, Atta HM, Samer H, Ahmed HH, Rashed LA, Sabry D, Abdel Raouf ER, Alkaffas MA - EXCLI J (2013)

Bottom Line: MSCs decreased the plaque lesions, heme oxygenase induction with stem cells also decreased plaque lesions however there was hemorrhage in the brain.Both heme oxygenase inducer alone or with stem cells increased seladin-1 expression and decreased cholesterol level.MSCs alone or with HO-1 induction exert a therapeutic effect against the brain lesion in Alzheimer's disease possibly through decreasing the brain cholesterol level and increasing seladin-1 gene expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Biochemistry, Unit of Biochemistry and Molecular Biology, Faculty of Medicine, Cairo University, Cairo, Egypt.

ABSTRACT
The objective is to evaluate the effect of heme oxygenase-1 (HO-1) enzyme inducer and inhibitor on Mesenchymal Stem Cells (MSCs) in Alzheimer disease. 70 female albino rats were divided equally into 7 groups as follows: group 1: healthy control; group 2: Aluminium chloride induced Alzheimer disease; group 3: induced Alzheimer rats that received intravenous injection of MSCs; group 4: induced Alzheimer rats that received MSCs and HO inducer cobalt protoporphyrin; group 5: induced Alzheimer rats that received MSCs and HO inhibitor zinc protoporphyrin; group 6: induced Alzheimer rats that received HO inducer; group7: induced Alzheimer rats that received HO inhibitor. Brain tissue was collected for HO-1, seladin-1 gene expression by real time polymerase chain reaction, heme oxygenase activity, cholesterol estimation and histopathological examination. MSCs decreased the plaque lesions, heme oxygenase induction with stem cells also decreased plaque lesions however there was hemorrhage in the brain. Both heme oxygenase inducer alone or with stem cells increased seladin-1 expression and decreased cholesterol level. MSCs alone or with HO-1 induction exert a therapeutic effect against the brain lesion in Alzheimer's disease possibly through decreasing the brain cholesterol level and increasing seladin-1 gene expression.

No MeSH data available.


Related in: MedlinePlus

Histopathological examination of brain tissues in different groups(A) Brain of control rat showing intact histological structure of the hippocampus(B) AD (H&EX60) showed multiple numbers of acellular plaques were detected in the mid brain, associated with oedema, hypoplasia, and congested blood capillary in the hippocampus.(C) AD+MSCs (H&EX60) showed congestion in the blood vessels and focal gliosis in the cerebral cortex.(D) AD+MSCs & inducer (H&EX60) showed congestion in the meninges, associated with focal hemorrhage and oedema with gliosis in the hippocampus.(E) AD+MSCs & inhibitor (H&EX60) showed diffuse gliosis in the cerebral cortex, associated with focal hemorrhage in the brain stem.(F) AD+ inducer (H&EX60) showed neuronal degeneration in the brain stem associated with focal gliosis in the cerebrum and congestion with hemorrhage in the hippocampus.(G) AD+inhibitor (H&EX60) showed focal gliosis with plague formation observed in the cerebrum, associated with atrophy and gliosis in the hippocampus.
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Figure 6: Histopathological examination of brain tissues in different groups(A) Brain of control rat showing intact histological structure of the hippocampus(B) AD (H&EX60) showed multiple numbers of acellular plaques were detected in the mid brain, associated with oedema, hypoplasia, and congested blood capillary in the hippocampus.(C) AD+MSCs (H&EX60) showed congestion in the blood vessels and focal gliosis in the cerebral cortex.(D) AD+MSCs & inducer (H&EX60) showed congestion in the meninges, associated with focal hemorrhage and oedema with gliosis in the hippocampus.(E) AD+MSCs & inhibitor (H&EX60) showed diffuse gliosis in the cerebral cortex, associated with focal hemorrhage in the brain stem.(F) AD+ inducer (H&EX60) showed neuronal degeneration in the brain stem associated with focal gliosis in the cerebrum and congestion with hemorrhage in the hippocampus.(G) AD+inhibitor (H&EX60) showed focal gliosis with plague formation observed in the cerebrum, associated with atrophy and gliosis in the hippocampus.

Mentions: Histopathological examination of the brain tissue of the AD group showed multiple acellular plaques in the mid brain, associated with oedema, hypoplasia, and congested blood capillary in the hippocampus (Figure 6B(Fig. 6)). Following MSCs injection there was congestion in the blood vessels and focal gliosis in the cerebral cortex (Figure 6C(Fig. 6)).With MSCs & HO inducer there was congestion in the meninges, associated with focal hemorrhage and oedema with gliosis in the hippocampus (Figure 6D(Fig. 6)). With MSCs & HO inhibitor there was diffuse gliosis in the cerebral cortex, associated with focal hemorrhage in the brain stem (Figure 6E(Fig. 6)). After injection of the inducer alone there was neuronal degeneration in the brain stem associated with focal gliosis in the cerebrum and congestion with hemorrhage in the hippocampus (Figure 6F(Fig. 6)). After injection of the inhibitor alone focal gliosis with plaque formation were observed in the cerebrum, associated with atrophy and gliosis in the hippocampus (Figure 6G(Fig. 6)).


Heme oxygenase effect on mesenchymal stem cells action on experimental Alzheimer's disease.

Abdel Aziza MT, Atta HM, Samer H, Ahmed HH, Rashed LA, Sabry D, Abdel Raouf ER, Alkaffas MA - EXCLI J (2013)

Histopathological examination of brain tissues in different groups(A) Brain of control rat showing intact histological structure of the hippocampus(B) AD (H&EX60) showed multiple numbers of acellular plaques were detected in the mid brain, associated with oedema, hypoplasia, and congested blood capillary in the hippocampus.(C) AD+MSCs (H&EX60) showed congestion in the blood vessels and focal gliosis in the cerebral cortex.(D) AD+MSCs & inducer (H&EX60) showed congestion in the meninges, associated with focal hemorrhage and oedema with gliosis in the hippocampus.(E) AD+MSCs & inhibitor (H&EX60) showed diffuse gliosis in the cerebral cortex, associated with focal hemorrhage in the brain stem.(F) AD+ inducer (H&EX60) showed neuronal degeneration in the brain stem associated with focal gliosis in the cerebrum and congestion with hemorrhage in the hippocampus.(G) AD+inhibitor (H&EX60) showed focal gliosis with plague formation observed in the cerebrum, associated with atrophy and gliosis in the hippocampus.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663655&req=5

Figure 6: Histopathological examination of brain tissues in different groups(A) Brain of control rat showing intact histological structure of the hippocampus(B) AD (H&EX60) showed multiple numbers of acellular plaques were detected in the mid brain, associated with oedema, hypoplasia, and congested blood capillary in the hippocampus.(C) AD+MSCs (H&EX60) showed congestion in the blood vessels and focal gliosis in the cerebral cortex.(D) AD+MSCs & inducer (H&EX60) showed congestion in the meninges, associated with focal hemorrhage and oedema with gliosis in the hippocampus.(E) AD+MSCs & inhibitor (H&EX60) showed diffuse gliosis in the cerebral cortex, associated with focal hemorrhage in the brain stem.(F) AD+ inducer (H&EX60) showed neuronal degeneration in the brain stem associated with focal gliosis in the cerebrum and congestion with hemorrhage in the hippocampus.(G) AD+inhibitor (H&EX60) showed focal gliosis with plague formation observed in the cerebrum, associated with atrophy and gliosis in the hippocampus.
Mentions: Histopathological examination of the brain tissue of the AD group showed multiple acellular plaques in the mid brain, associated with oedema, hypoplasia, and congested blood capillary in the hippocampus (Figure 6B(Fig. 6)). Following MSCs injection there was congestion in the blood vessels and focal gliosis in the cerebral cortex (Figure 6C(Fig. 6)).With MSCs & HO inducer there was congestion in the meninges, associated with focal hemorrhage and oedema with gliosis in the hippocampus (Figure 6D(Fig. 6)). With MSCs & HO inhibitor there was diffuse gliosis in the cerebral cortex, associated with focal hemorrhage in the brain stem (Figure 6E(Fig. 6)). After injection of the inducer alone there was neuronal degeneration in the brain stem associated with focal gliosis in the cerebrum and congestion with hemorrhage in the hippocampus (Figure 6F(Fig. 6)). After injection of the inhibitor alone focal gliosis with plaque formation were observed in the cerebrum, associated with atrophy and gliosis in the hippocampus (Figure 6G(Fig. 6)).

Bottom Line: MSCs decreased the plaque lesions, heme oxygenase induction with stem cells also decreased plaque lesions however there was hemorrhage in the brain.Both heme oxygenase inducer alone or with stem cells increased seladin-1 expression and decreased cholesterol level.MSCs alone or with HO-1 induction exert a therapeutic effect against the brain lesion in Alzheimer's disease possibly through decreasing the brain cholesterol level and increasing seladin-1 gene expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Biochemistry, Unit of Biochemistry and Molecular Biology, Faculty of Medicine, Cairo University, Cairo, Egypt.

ABSTRACT
The objective is to evaluate the effect of heme oxygenase-1 (HO-1) enzyme inducer and inhibitor on Mesenchymal Stem Cells (MSCs) in Alzheimer disease. 70 female albino rats were divided equally into 7 groups as follows: group 1: healthy control; group 2: Aluminium chloride induced Alzheimer disease; group 3: induced Alzheimer rats that received intravenous injection of MSCs; group 4: induced Alzheimer rats that received MSCs and HO inducer cobalt protoporphyrin; group 5: induced Alzheimer rats that received MSCs and HO inhibitor zinc protoporphyrin; group 6: induced Alzheimer rats that received HO inducer; group7: induced Alzheimer rats that received HO inhibitor. Brain tissue was collected for HO-1, seladin-1 gene expression by real time polymerase chain reaction, heme oxygenase activity, cholesterol estimation and histopathological examination. MSCs decreased the plaque lesions, heme oxygenase induction with stem cells also decreased plaque lesions however there was hemorrhage in the brain. Both heme oxygenase inducer alone or with stem cells increased seladin-1 expression and decreased cholesterol level. MSCs alone or with HO-1 induction exert a therapeutic effect against the brain lesion in Alzheimer's disease possibly through decreasing the brain cholesterol level and increasing seladin-1 gene expression.

No MeSH data available.


Related in: MedlinePlus