Ginsenoside-Rg1 combined with a conditioned medium from induced neuron-like hUCMSCs alleviated the apoptosis in a cell model of ALS through regulating the NF-κB/Bcl-2 pathway.
10.1016/S1875-5364(23)60445-5
- Author:
Yu HUANG
1
,
2
,
3
,
4
;
Huili YANG
1
,
2
,
3
,
5
;
Biying YANG
1
,
2
,
3
,
5
;
Yu ZHENG
1
,
2
,
3
,
5
;
Xiaomei HOU
1
,
2
,
3
,
5
;
Guiling CHEN
1
,
2
,
3
,
4
;
Wenqi ZHANG
1
,
2
,
3
,
5
;
Xiang ZENG
1
,
2
,
3
,
4
;
Baoxin DU
1
,
2
,
3
,
6
Author Information
1. Labortory of Stem Cell Clinical Reaearch, The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou 510006, China
2. Labortory of Stem Cell Biology and Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510006, China
3. Labortory of Stem Cell Biology and Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou 510006, China
4. Labortory of Stem Cell Clinical Research, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510006, China.
5. Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510006, China.
6. Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510006, China. Electronic address: dbx.dr@163.com.
- Publication Type:Journal Article
- Keywords:
Amyotrophic lateral sclerosis;
Apoptosis;
Conditioned medium;
Ginsenoside-Rg1;
Umbilical cord mesenchymal stem cells
- MeSH:
Humans;
NF-kappa B/metabolism*;
Ginsenosides/pharmacology*;
Amyotrophic Lateral Sclerosis/genetics*;
Culture Media, Conditioned/pharmacology*;
Superoxide Dismutase-1;
Neurodegenerative Diseases;
Neurons/metabolism*;
Apoptosis
- From:
Chinese Journal of Natural Medicines (English Ed.)
2023;21(7):540-550
- CountryChina
- Language:English
-
Abstract:
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting both upper and lower motor neurons in the brain and spinal cord. One important aspect of ALS pathogenesis is superoxide dismutase 1 (SOD1) mutant-mediated mitochondrial toxicity, leading to apoptosis in neurons. This study aimed to evaluate the neural protective synergistic effects of ginsenosides Rg1 (G-Rg1) and conditioned medium (CM) on a mutational SOD1 cell model, and to explore the underlying mechanisms. We found that the contents of nerve growth factor, glial cell line-derived neurotrophic factor, and brain-derived neurotrophic factor significantly increased in CM after human umbilical cord mesenchymal stem cells (hUCMSCs) were exposed to neuron differentiation reagents for seven days. CM or G-Rg1 decreased the apoptotic rate of SOD1G93A-NSC34 cells to a certain extent, but their combination brought about the least apoptosis, compared with CM or G-Rg1 alone. Further research showed that the anti-apoptotic protein Bcl-2 was upregulated in all the treatment groups. Proteins associated with mitochondrial apoptotic pathways, such as Bax, caspase 9 (Cas-9), and cytochrome c (Cyt c), were downregulated. Furthermore, CM or G-Rg1 also inhibited the activation of the nuclear factor-kappa B (NF-κB) signaling pathway by reducing the phosphorylation of p65 and IκBα. CM/G-Rg1 or their combination also reduced the apoptotic rate induced by betulinic acid (BetA), an agonist of the NF-κB signaling pathway. In summary, the combination of CM and G-Rg1 effectively reduced the apoptosis of SOD1G93A-NSC34 cells through suppressing the NF-κB/Bcl-2 signaling pathway (Fig. 1 is a graphical representation of the abstract).
