Modulation of Glial Responses by Furanocembranolides: Leptolide Diminishes Microglial Inflammation in Vitro and Ameliorates Gliosis In Vivo in a Mouse Model of Obesity and Insulin Resistance.
Miriam Corraliza-GómezAmalia B GallardoAlfredo MorenoJosé M de la RosaLuis D'CrozJosé DariasEduardo ArranzIrene Cózar-CastellanoMaría D GanforninaMercedes CuetoPublished in: Marine drugs (2020)
Neurodegenerative diseases are age-related disorders caused by progressive neuronal death in different regions of the nervous system. Neuroinflammation, modulated by glial cells, is a crucial event during the neurodegenerative process; consequently, there is an urgency to find new therapeutic products with anti-glioinflammatory properties. Five new furanocembranolides (1-5), along with leptolide, were isolated from two different extracts of Leptogorgia sp., and compound 6 was obtained from chemical transformation of leptolide. Their structures were determined based on spectroscopic evidence. These seven furanocembranolides were screened in vitro by measuring their ability to modulate interleukin-1β (IL-1β) production by microglial BV2 cells after LPS (lipopolysaccharide) stimulation. Leptolide and compounds 3, 4 and 6 exhibited clear anti-inflammatory effects on microglial cells, while compound 2 presented a pro-inflammatory outcome. The in vitro results prompted us to assess anti-glioinflammatory effects of leptolide in vivo in a high-fat diet-induced obese mouse model. Interestingly, leptolide treatment ameliorated both microgliosis and astrogliosis in this animal model. Taken together, our results reveal a promising direct biological effect of furanocembranolides on microglial cells as bioactive anti-inflammatory molecules. Among them, leptolide provides us a feasible therapeutic approach to treat neuroinflammation concomitant with metabolic impairment.
Keyphrases
- induced apoptosis
- insulin resistance
- lps induced
- lipopolysaccharide induced
- inflammatory response
- mouse model
- cell cycle arrest
- high fat diet induced
- anti inflammatory
- metabolic syndrome
- neuropathic pain
- adipose tissue
- oxidative stress
- type diabetes
- gene expression
- traumatic brain injury
- cell death
- weight loss
- toll like receptor
- high fat diet
- multiple sclerosis
- high resolution
- physical activity
- polycystic ovary syndrome
- pi k akt
- cell proliferation
- bariatric surgery
- mass spectrometry
- weight gain
- combination therapy