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Scolopendra subspinipes mutilans attenuates neuroinflammation in symptomatic hSOD1(G93A) mice.

Cai M, Choi SM, Song BK, Son I, Kim S, Yang EJ - J Neuroinflammation (2013)

Bottom Line: However, the mechanisms underlying the effects of SSM are currently unclear, even though SSM increases immune and antibiotic activity.We found that SSM treatment attenuated the loss of motor neurons and reduced the activation of microglial cells and astrocytes.Furthermore, we demonstrated that SSM administration in this animal model of ALS suppressed oxidative stress in the brainstem and spinal cord by 1.6- and 1.8-fold, respectively.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Medial Research, Korea Institute of Oriental Medicine, 483 Expo-ro, Yuseong-gu, Daejeon 305-811, Republic of Korea. kscndl@hanmail.net.

ABSTRACT

Background: Amyotrophic lateral sclerosis (ALS) is a progressive, adult-onset neurodegenerative disorder characterized by selective motor neuron death in the spinal cord, brainstem, and motor cortex. Neuroinflammation is one of several pathological causes of degenerating motor neurons and is induced by activated microglial cells and astrocytes in ALS.Scolopendra subspinipes mutilans (SSM) is utilized in traditional Chinese and Korean medicine for the treatment of a variety of diseases, such as cancer, apoplexy, and epilepsy. However, the mechanisms underlying the effects of SSM are currently unclear, even though SSM increases immune and antibiotic activity.

Methods: To determine the effects of SSM on symptomatic hSOD1G93A transgenic mice, SSM (2.5 μℓ/g) was injected bilaterally at the Zusanli (ST36) acupoint three times per week for two weeks. The effects of SSM treatment on anti-neuroinflammation in the brainstem and spinal cord of hSOD1G93A mice were assessed via Nissl and Fluoro-Jade B (FJB) staining, and immunohistochemistry using Iba-1, CD14, HO1, and NQO1 proteins was evaluated by Western blotting.

Results: In this study, we investigated whether SSM affects neuroinflammation in the spinal cord of symptomatic hSOD1G93A transgenic mice. We found that SSM treatment attenuated the loss of motor neurons and reduced the activation of microglial cells and astrocytes. Furthermore, we demonstrated that SSM administration in this animal model of ALS suppressed oxidative stress in the brainstem and spinal cord by 1.6- and 1.8-fold, respectively.

Conclusions: Our findings suggest that SSM, which has previously been used in complementary and alternative medicine (CAM), might also be considered as an anti-neuroinflammatory therapy for neurodegenerative diseases.

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SSM treatment increases motor neuron survival in hSOD1G93A mice. SSM (2.5 μℓ/g) was administered bilaterally at acupoint ST36 three times per week for two weeks. Photomicrographs of Nissl (A) and FJB (C) staining of the lumbar spinal cord. Each right-hand column depicts a magnified image of the rectangular region of the corresponding image in the left column. The numbers of viable motor neurons (B) and degenerating FJB-positive glial cells (D) were counted, as described in the magnified spinal cord column. (E) Photomicrographs of MAP2 staining of the lumbar spinal cord. Each right-hand column depicts a magnified image of the rectangular region of the corresponding image in the left column. (F) Quantitative analysis of MAP2-positive cells each magnified column. Control (Sal) animals were bilaterally injected with an equivalent volume of saline at the ST36 acupoint. The data are presented as the means ± SEM (N = 6 animals/genotype). Statistical significance was assessed via t-test. ***P < 0.001 compared to the saline-treated group. Magnification: 100×. Bar = 500 μm. Sal: saline-treated hSOD1G93A mice, SSM: Scolopendra subspinipes mutilans (SSM)-treated hSOD1G93A mice.
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Figure 1: SSM treatment increases motor neuron survival in hSOD1G93A mice. SSM (2.5 μℓ/g) was administered bilaterally at acupoint ST36 three times per week for two weeks. Photomicrographs of Nissl (A) and FJB (C) staining of the lumbar spinal cord. Each right-hand column depicts a magnified image of the rectangular region of the corresponding image in the left column. The numbers of viable motor neurons (B) and degenerating FJB-positive glial cells (D) were counted, as described in the magnified spinal cord column. (E) Photomicrographs of MAP2 staining of the lumbar spinal cord. Each right-hand column depicts a magnified image of the rectangular region of the corresponding image in the left column. (F) Quantitative analysis of MAP2-positive cells each magnified column. Control (Sal) animals were bilaterally injected with an equivalent volume of saline at the ST36 acupoint. The data are presented as the means ± SEM (N = 6 animals/genotype). Statistical significance was assessed via t-test. ***P < 0.001 compared to the saline-treated group. Magnification: 100×. Bar = 500 μm. Sal: saline-treated hSOD1G93A mice, SSM: Scolopendra subspinipes mutilans (SSM)-treated hSOD1G93A mice.

Mentions: To determine whether SSM treatment affects neuronal loss in the spinal cord of symptomatic hSOD1G93A transgenic mice, we performed a histochemical assessment of lumbar spinal cord sections in SSM- and saline-treated mice. As shown in Figure 1A-B, we demonstrated via Nissl staining that the administration of SSM attenuated motor neuron loss in the ventral horn of L4-L5 segments of the spinal cord by 3.4-fold. To confirm the reduction of motor neuron loss induced by SSM treatment, we quantified the number of degenerated neurons through FB-J staining. As shown in Figure 1C-D, compared to age-matched control mice, the number of degenerated neurons in the ventral horn of the spinal cord was reduced by 4.6-fold in SSM-treated hSOD1G93A transgenic mice. In addition, using an MAP2 antibody, we observed that neuronal cells were increased by 1.2-fold in the spinal cord of SSM-treated hSOD1G93A mice compared to the saline-treated control mice (Figure 1E-F).


Scolopendra subspinipes mutilans attenuates neuroinflammation in symptomatic hSOD1(G93A) mice.

Cai M, Choi SM, Song BK, Son I, Kim S, Yang EJ - J Neuroinflammation (2013)

SSM treatment increases motor neuron survival in hSOD1G93A mice. SSM (2.5 μℓ/g) was administered bilaterally at acupoint ST36 three times per week for two weeks. Photomicrographs of Nissl (A) and FJB (C) staining of the lumbar spinal cord. Each right-hand column depicts a magnified image of the rectangular region of the corresponding image in the left column. The numbers of viable motor neurons (B) and degenerating FJB-positive glial cells (D) were counted, as described in the magnified spinal cord column. (E) Photomicrographs of MAP2 staining of the lumbar spinal cord. Each right-hand column depicts a magnified image of the rectangular region of the corresponding image in the left column. (F) Quantitative analysis of MAP2-positive cells each magnified column. Control (Sal) animals were bilaterally injected with an equivalent volume of saline at the ST36 acupoint. The data are presented as the means ± SEM (N = 6 animals/genotype). Statistical significance was assessed via t-test. ***P < 0.001 compared to the saline-treated group. Magnification: 100×. Bar = 500 μm. Sal: saline-treated hSOD1G93A mice, SSM: Scolopendra subspinipes mutilans (SSM)-treated hSOD1G93A mice.
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Figure 1: SSM treatment increases motor neuron survival in hSOD1G93A mice. SSM (2.5 μℓ/g) was administered bilaterally at acupoint ST36 three times per week for two weeks. Photomicrographs of Nissl (A) and FJB (C) staining of the lumbar spinal cord. Each right-hand column depicts a magnified image of the rectangular region of the corresponding image in the left column. The numbers of viable motor neurons (B) and degenerating FJB-positive glial cells (D) were counted, as described in the magnified spinal cord column. (E) Photomicrographs of MAP2 staining of the lumbar spinal cord. Each right-hand column depicts a magnified image of the rectangular region of the corresponding image in the left column. (F) Quantitative analysis of MAP2-positive cells each magnified column. Control (Sal) animals were bilaterally injected with an equivalent volume of saline at the ST36 acupoint. The data are presented as the means ± SEM (N = 6 animals/genotype). Statistical significance was assessed via t-test. ***P < 0.001 compared to the saline-treated group. Magnification: 100×. Bar = 500 μm. Sal: saline-treated hSOD1G93A mice, SSM: Scolopendra subspinipes mutilans (SSM)-treated hSOD1G93A mice.
Mentions: To determine whether SSM treatment affects neuronal loss in the spinal cord of symptomatic hSOD1G93A transgenic mice, we performed a histochemical assessment of lumbar spinal cord sections in SSM- and saline-treated mice. As shown in Figure 1A-B, we demonstrated via Nissl staining that the administration of SSM attenuated motor neuron loss in the ventral horn of L4-L5 segments of the spinal cord by 3.4-fold. To confirm the reduction of motor neuron loss induced by SSM treatment, we quantified the number of degenerated neurons through FB-J staining. As shown in Figure 1C-D, compared to age-matched control mice, the number of degenerated neurons in the ventral horn of the spinal cord was reduced by 4.6-fold in SSM-treated hSOD1G93A transgenic mice. In addition, using an MAP2 antibody, we observed that neuronal cells were increased by 1.2-fold in the spinal cord of SSM-treated hSOD1G93A mice compared to the saline-treated control mice (Figure 1E-F).

Bottom Line: However, the mechanisms underlying the effects of SSM are currently unclear, even though SSM increases immune and antibiotic activity.We found that SSM treatment attenuated the loss of motor neurons and reduced the activation of microglial cells and astrocytes.Furthermore, we demonstrated that SSM administration in this animal model of ALS suppressed oxidative stress in the brainstem and spinal cord by 1.6- and 1.8-fold, respectively.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Medial Research, Korea Institute of Oriental Medicine, 483 Expo-ro, Yuseong-gu, Daejeon 305-811, Republic of Korea. kscndl@hanmail.net.

ABSTRACT

Background: Amyotrophic lateral sclerosis (ALS) is a progressive, adult-onset neurodegenerative disorder characterized by selective motor neuron death in the spinal cord, brainstem, and motor cortex. Neuroinflammation is one of several pathological causes of degenerating motor neurons and is induced by activated microglial cells and astrocytes in ALS.Scolopendra subspinipes mutilans (SSM) is utilized in traditional Chinese and Korean medicine for the treatment of a variety of diseases, such as cancer, apoplexy, and epilepsy. However, the mechanisms underlying the effects of SSM are currently unclear, even though SSM increases immune and antibiotic activity.

Methods: To determine the effects of SSM on symptomatic hSOD1G93A transgenic mice, SSM (2.5 μℓ/g) was injected bilaterally at the Zusanli (ST36) acupoint three times per week for two weeks. The effects of SSM treatment on anti-neuroinflammation in the brainstem and spinal cord of hSOD1G93A mice were assessed via Nissl and Fluoro-Jade B (FJB) staining, and immunohistochemistry using Iba-1, CD14, HO1, and NQO1 proteins was evaluated by Western blotting.

Results: In this study, we investigated whether SSM affects neuroinflammation in the spinal cord of symptomatic hSOD1G93A transgenic mice. We found that SSM treatment attenuated the loss of motor neurons and reduced the activation of microglial cells and astrocytes. Furthermore, we demonstrated that SSM administration in this animal model of ALS suppressed oxidative stress in the brainstem and spinal cord by 1.6- and 1.8-fold, respectively.

Conclusions: Our findings suggest that SSM, which has previously been used in complementary and alternative medicine (CAM), might also be considered as an anti-neuroinflammatory therapy for neurodegenerative diseases.

Show MeSH
Related in: MedlinePlus