Many scientists are interested in anti-aging interventions and seek to identify anti-aging medicines. In our previous study, we reported that an antitussive drug, tipepidine (TIP), activates AMP-activated protein kinase (AMPK) and improves glucose intolerance in high-fat diet-induced obese mice. Activation of AMPK has been reported to extend lifespan in various experimental organisms, including Caenorhabditis elegans. In this study, we examined whether TIP extends lifespan in C. elegans via AMPK activation. TIP treatment (50–100 μM) extended the median lifespan of wild-type C. elegans (N2), but not that of the AMPK catalytic subunit mutant aak-2(rr48). These results suggest that TIP extends lifespan in C. elegans in an AMPK-dependent manner.

Plasminogen activator inhibitor-1 (PAI-1) is a serine protease inhibitor that controls trophoblast invasion by inhibiting fibrinolysis at the feto-maternal interface. This study aimed to compare PAI-1 expression patterns in decidual cells between different abortion types and investigate the role of PAI-1 in early pregnancy. Missed abortion (n = 22) and incomplete abortion (n = 16) cases were compared with induced abortion serving as normal pregnancy control (n = 16). PAI-1 localization and expression levels were evaluated using immunohistochemistry. PAI-1 was distributed in the cytoplasm of decidual cells. In addition, many PAI-1-positive cells were observed in the decidua basalis just under the Nitabuch fibrinoid layer, where many extravillous trophoblasts (EVTs) invaded. The percentage of PAI-1-positive decidual cells was not reduced in missed abortion (49.7 ± 29.6%) but was significantly reduced in incomplete abortion (11.6 ± 12.6%) compared to induced abortion as control (44.4 ± 10.9%). The significant reduction of PAI-1-positive decidual cells in incomplete abortion, which is characterized by bleeding, suggests that PAI-1 deficiency may cause excessive fibrinolysis leading to this clinical outcome.

This study aimed to elucidate the mechanism underlying tolerance to the sedative effects of propofol, focusing on cannabinoid 1 (CB1) receptor regulation. Male Wistar rats received continuous propofol infusion (30–40 mg/kg/h) for 1, 2, 4, or 12 h prior to tissue collection. Brain regions including the cortex, hippocampus, striatum, brain stem, and cerebellum were analyzed. Changes in CB1 receptor mRNA transcript abundance were assessed using semi-quantitative PCR. Across all examined regions, CB1 receptor mRNA levels showed a time-dependent decrease following propofol administration. Reductions were detectable as early as 1 h and became more pronounced at 4 and 12 h. This downregulation was consistently observed across multiple brain regions, suggesting a widespread effect rather than region-specific modulation. These findings suggest that continuous propofol exposure leads to significant downregulation of CB1 receptor expression, which may contribute to receptor desensitization and the development of tolerance to its sedative effects. Modulation of the endocannabinoid system may therefore play a key role in propofol-induced tolerance.