PubMed · 11763800
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2001-12-01. Eflornithine.. https://doi.org/10.1093/ajhp%2F58.23.2244
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Posttraumatic stress disorder (PTSD) is characterized by traumatic memories that can manifest as daytime recollections, traumatic nightmares, or flashbacks in which components of the event are relieved. These symptoms reflect excessive retrieval of traumatic memories that often retain their vividness and power to evoke distress for decades or even a lifetime. We have reported previously that elevated glucocorticoid levels inhibit memory retrieval in animals and healthy human subjects. We therefore hypothesized that the administration of cortisol might also inhibit the retrieval of traumatic memories in patients with PTSD. In a recent pilot study, we found the first evidence to support this hypothesis. During a 3-month observation period, low-dose cortisol (10 mg/day) was administered orally for 1 month to three patients with chronic PTSD using a double-blind, placebo-controlled, crossover design. In each patient investigated, there was a significant treatment effect with cortisol-related reductions in one of the daily rated symptoms of traumatic memories without causing adverse side effects. Future studies with more patients and longer treatment periods are required to evaluate the efficacy of cortisol treatment for PTSD.
This study was aimed to investigate the influence of PPARalpha agonist on the expression of TF (tissue factor) in THP-1 cells. THP-1 cells were pretreated with different concentrations of PPARalpha agonist (fenofibrate) for definite time. Lipopolysaccharide (LPS)-induced TF mRNA and protein levels were detected by RT-PCR and Western blot respectively. The results showed that fenofibrate decreased tissue factor protein and mRNA expression in supernatants of LPS-stimulated human monocytes in a concentration-dependent manner (P < 0.05 - 0.01, n = 5). It is concluded that fenofibrate inhibit TF expression induced by LPS in THP-1 cells, which may be involved in the anti-atherosclerotic effects of PPARalpha agonist.
Wen-Pi-Tang, an Oriental medical prescription composed of Rhei Rhizoma, Ginseng Radix, Aconiti Tuber, Zingiberis Rhizoma and Glycyrrhizae Radix, is used clinically as a medicine to treat renal failure. This study was conducted to examine the inhibitory activity of the five crude drug components of Wen-Pi-Tang and several pure compounds isolated from Rhei Rhizoma and Glycyrrhizae Radix against the protein glycation reaction. Rhei Rhizoma exerted the most potent activity, Zingiberis Rhizoma and Glycyrrhizae Radix showed relatively moderate activity, whereas Aconiti Tuber and Ginseng Radix showed weak activity. On the other hand, of 20 compounds obtained from Rhei Rhizoma and Glycyrrhizae Radix, tannins, especially rhatannin, RG-tannin and procyanidin B-2 3,3'-di-O-gallate, showed significantly strong activities that were more effective than the positive control, aminoguanidine. Some flavones such as licochalcone A and licochalcone B, and anthraquinones such as emodin and aloe-emodin, also showed inhibitory activity. These findings may help to explain, at least in part, certain pharmacological activities of Wen-Pi-Tang, whose clinical efficacy against renal failure is already recognized.