Arctigenin derivative A-1 ameliorates motor dysfunction and pathological manifestations in SOD1 G93A transgenic mice via the AMPK/SIRT1/PGC-1α and AMPK/SIRT1/IL-1β/NF-κB pathways.
Bocheng XiongChao YangXiao YangSong LuoShangming LiChongyang ChenKaiwu HeLulin NiePeimao LiShupeng LiHaiyan HuangJianjun LiuZaijun ZhangYongmei XieLiangyu ZouXifei YangPublished in: CNS neuroscience & therapeutics (2024)
A-1 treatment reduced motor neuron loss, improved gastrocnemius atrophy, and delayed ALS progression through the AMPK/SIRT1/PGC-1α pathway, which promotes mitochondrial biogenesis. Furthermore, the AMPK/SIRT1/IL-1β/NF-κB pathway exerted neuroprotective effects by reducing neuroinflammation. These findings suggest A-1 as a promising therapeutic approach for ALS.
Keyphrases
- oxidative stress
- skeletal muscle
- ischemia reperfusion injury
- lps induced
- amyotrophic lateral sclerosis
- signaling pathway
- protein kinase
- traumatic brain injury
- inflammatory response
- nuclear factor
- lipopolysaccharide induced
- cognitive impairment
- cell proliferation
- blood brain barrier
- combination therapy
- replacement therapy