Sesamolin

Int J Biomed Sci. 2006 Sep; 2(3): 284–8.

Neuroprotective Effects of Sesamin and Sesamolin on Gerbil Brain in Cerebral Ischemia[Pubmed: 23674992]

Sesamin and Sesamolin, abundant lignans found in sesame oil, have been demonstrated to possess several bioactivities beneficial for human health.
METHODS AND RESULTS:
Excess generation of nitric oxide in lipopolysaccharide-stimulated rat primary microglia cells was significantly attenuated when they were pretreated with sesamin or Sesamolin. The neuroprotective effect of sesamin and Sesamolin was also observed in vivo using gerbils subjected to a focal cerebral ischemia induced by occlusion of the right common carotid artery and the right middle cerebral artery. Repeated treatment of sesamin or a crude sesame oil extract containing both sesamin and Sesamolin significantly reduced the infarct size, visualized via 2,3,5-triphenyltetrazolium chloride staining, by approximately 50% when compared with the control group.
CONCLUSIONS:
These results suggest that sesamin and Sesamolin exert effective neuroprotection against cerbral ischemia.

Br J Nutr. 2007 Jan;97(1):85-95.

Comparative analysis of sesame lignans (sesamin and sesamolin) in affecting hepatic fatty acid metabolism in rats.[Pubmed: 17217563]

Effects of sesamin and Sesamolin (sesame lignans) on hepatic fatty acid metabolism were compared in rats.
METHODS AND RESULTS:
Rats were fed either a lignan-free diet, a diet containing 0.6 or 2 g/kg lignan (sesamin or Sesamolin), or a diet containing both sesamin (1.4 g/kg) and Sesamolin (0.6 g/kg) for 10 d. Sesamin and Sesamolin dose-dependently increased the activity and mRNA abundance of various enzymes involved in hepatic fatty acid oxidation. The increase was much greater with Sesamolin than with sesamin. These lignans increased parameters of hepatic fatty acid oxidation in an additive manner when added simultaneously to an experimental diet. In contrast, they decreased the activity and mRNA abundance of hepatic lipogenic enzymes despite dose-dependent effects not being necessarily obvious. Sesamin and Sesamolin were equally effective in lowering parameters of lipogenesis. Sesamolin accumulated in serum at 33- and 46-fold the level of sesamin at dietary concentrations of 0.6 and 2 g/kg, respectively. The amount of Sesamolin accumulated in liver was 10- and 7-fold that of sesamin at the respective dietary levels. Sesamolin rather than sesamin can account for the potent physiological effect of sesame seeds in increasing hepatic fatty acid oxidation observed previously. Differences in bioavailability may contribute to the divergent effects of sesamin and Sesamolin on hepatic fatty acid oxidation.
CONCLUSIONS:
Sesamin compared to Sesamolin was more effective in reducing serum and liver lipid levels despite Sesamolin more strongly increasing hepatic fatty acid oxidation.

J Neurosci Res. 2003 Oct 1;74(1):123-33.

Protective effects of sesamin and sesamolin on hypoxic neuronal and PC12 cells.[Pubmed: 13130514 ]

Reactive oxygen species (ROS) are important mediators of a variety of pathological processes, including inflammation and ischemic injury. The neuroprotective effects of sesame antioxidants, sesamin and Sesamolin, against hypoxia or H2O2-induced cell injury were evaluated by cell viability or lactate dehydrogenase (LDH) activity.
METHODS AND RESULTS:
Sesamin and Sesamolin reduced LDH release of PC12 cells under hypoxia or H2O2-stress in a dose-dependent manner. Dichlorofluorescein (DCF)-sensitive ROS production was induced in PC12 cells by hypoxia or H2O2-stress but was diminished in the presence of sesamin and Sesamolin. We evaluated further the role of mitogen-activated protein kinases (MAPKs) and caspase-3 in hypoxia-induced PC12 cell death. Extracellular signal-regulated protein kinase (ERK) 1, c-jun N-terminal kinase (JNK), and p38 MAPKs of signaling pathways were activated during hypoxia. We found that the inhibition of MAPKs and caspase-3 by sesamin and Sesamolin correlated well with the reduction in LDH release under hypoxia. Furthermore, the hypoxia-induced apoptotic-like cell death in cultured cortical cells as detected by a fluorescent DNA binding dye was reduced significantly by sesamin and Sesamolin.
CONCLUSIONS:
Taken together, these results suggest that the protective effect of sesamin and Sesamolin on hypoxic neuronal and PC12 cells might be related to suppression of ROS generation and MAPK activation.

J Nutr. 1998 Jun;128(6):1018-22.

Sesamolin inhibits lipid peroxidation in rat liver and kidney.[Pubmed: 9614163]

Although the sesame lignans, sesaminol and Sesamolinol, have been shown to possess antioxidative activity, less is known about the metabolism and antioxidative properties of Sesamolin, a major constituent of sesame oil.
METHODS AND RESULTS:
To determine the ability of Sesamolin to act as an antioxidant in vivo, we fed rats a diet containing 1% Sesamolin for 2 wk and studied its metabolism and its effects on oxidative stress. About 75% of the ingested Sesamolin was excreted unmetabolized in feces, but it was not detected in urine. Sesamolin and its metabolites, sesamol and Sesamolinol, were excreted primarily as sulfates and glucuronides. The amount of Sesamolin and its metabolites was lower in the plasma than in the liver or kidneys. When we compared rats fed a diet containing 1% Sesamolin for 14 d with those fed a control diet, we found that liver weight was significantly greater in the former group. Lipid peroxidation activity, measured as 2-thiobarbituric acid reactive substances, was significantly lower in the kidneys and liver of the Sesamolin-fed rats than in the controls. In addition, the amount of 8-hydroxy-2'-deoxyguanosine excreted in the urine was significantly lower in the Sesamolin-fed rats.
CONCLUSIONS:
These results suggest that Sesamolin and its metabolites may contribute to the antioxidative properties of sesame seeds and oil and support our hypothesis that sesame lignans reduce susceptibility to oxidative stress.