In this study, ginkgo biloba leaf extract (GBE) was added to sample cigarettes, including in the filter (0.8 mg/cigarette) and/or the cut filler (0.8 mg/cigarette). The effects of GBE in scavenging free radicals and reducing mutagenicity and toxicity of cigarette smoke in vivo were investigated. Smoke analysis results indicated that GBE eliminated up to 30% of free radicals. Biological experiments, conducted for both GBE cigarettes and control samples, included the Ames test, acute toxicity, neutral red cytotoxicity assay and chronic toxicity. Results showed that the mutagenicity and toxicity of the GBE cigarettes were lower than for the control cigarettes. A possible mechanism of GBE in scavenging free radicals is discussed in this article.
Two protoporphyrin derivatives were prepared by a facile method using inexpensive hemin as starting material. They were added to cigarette filters to reduce the carcinogenic tobacco specific N-nitroamines (TSNAs), especially toward NNK (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) and NNN (N-nitrosonornicotine) for environment protection and public health. The reduction level of TSNAs was reached to 37.6% from MSS, with greater reductions when more porphyrin was included in the filter. The decrease level for NNK by protoporphyrin derivatives is more effective than NNN. The interaction between protoporphyrin derivatives and TSNAs (NNK and NNN) were investigated by fluorescence spectra and UV-visible titration. The correlation coefficients were 0.978~0.997 and the binding constants was the scope from 1.26 × 103 to 4.04 × 104. The interaction mechanisms between protoporphyrin derivatives and, NNK and NNN are possibly the co-interaction of hydrogen bond binding and strong π–π stacking.
Gut microbiota are very important for energy metabolism and regulation, which in turn affect the health and physiological functions of the host. The most direct way to change the gut microbiota is to supplement with probiotics. In this study, we screened Lactobacillus plantarum (PL-02), a probiotic of human-origin, from the intestines of Olympic gold medalists and explored the role of PL-02 in improved exercise endurance performance, reduced fatigue biochemical parameters, and changes in body composition. Male Institute of Cancer Research (ICR) mice were assigned to 0 CFU/kg (vehicle), 2.05 × 109 CFU/kg (PL-02-1X), 4.10 × 109 CFU/kg (PL-02-2X), and 1.03 × 1010 CFU/kg (PL-02-5X) groups and were fed by oral gavage once daily for 4 weeks to assess exercise performance, fatigue parameters, and body composition. The results showed that 4 weeks of PL-02 supplementation could significantly increase muscle mass, improve muscle strength and endurance performance, and increase hepatic and muscular glycogen storage. Furthermore, PL-02 could significantly decrease fatigue biochemical parameters, such as lactate, blood urea nitrogen (BUN), ammonia, and creatine kinase (CK) levels, after exercise. We believe that PL-02 can be used as a supplement to improve exercise performance and for its anti-fatigue effect.
Background: Expression of translocator protein (TSPO) on the outer mitochondrial membrane of activated microglia is strongly associated with neuroinflammation. The second-generation PET ligand [18F]FEPPA specifically binds TSPO to enable in vivo visualization and quantification of neuroinflammation. We optimized an fully automated radiosynthesis method and evaluated the utility of [18F]FEPPA, the second-generation PET ligand specifically binds TSPO, in a mouse model of systemic LPS challenge to detect TSPO-associated signals of central and peripheral inflammation. In vivo dynamic PET/MR imaging was performed in LPS-induced and control mice after [18F]FEPPA administration. The relationship between the [18F]FEPPA signal and the dose of LPS was assessed. The cytokine levels (i.e. TNF-α, Il-1β, Il-6) in LPS-induced mice were measured by RT-PCR. Standard uptake value (SUV), total volume of distribution (VT) and area under the curve (AUC) were determined based on the metabolite-uncorrected plasma input function. Western blotting and immunostaining were used to measure TSPO expression in the brain. Results: The fully automated [18F]FEPPA radiosynthesis produced an uncorrected radiochemical yield of 30 ± 2% within 80 min, with a radiochemical purity greater than 99% and specific activity of 148.9‒216.8 GBq/µmol. Significant differences were observed in the brain after [18F]FEPPA administration: SUV, VT, and AUC were 1.61 ± 0.1, 1.25 ± 0.12, and 1.58 ± 0.09-fold higher in LPS-injected mice than controls. TNF-α, Il-1β and Il-6 mRNA levels were also elevated in the brains of LPS-injected mice. Western blotting revealed TSPO (p<0.05) and Iba-1 (p<0.01) were upregulated in the brain after LPS administration. In LPS-injected mice, TSPO immunoactivity colocalized with Iba-1 in the cerebrum and TSPO was significantly overexpressed in the hippocampus and cerebellum. The peripheral organs (heart, lung) of LPS-injected mice had higher [18F]FEPPA signal-to-noise ratios than control mice. Conclusions: Based on the robust data on ligand specificity and selectivity in both central and peripheral tissues using 7T PET/MR imaging, we demonstrate that the high affinity, stability and high-contrast visualization indicate detection of TSPO using [18F]FEPPA represents a promising, specific biomarker for early diagnosis and neuropathological follow-up of neuroinflammatory processes.
Plexins are semaphorin receptors that play essential roles in neuronal axon guidance and in many other important biological processes. Plexin signaling depends on a semaphorin-induced dimerization mechanism, and is modulated by small signaling GTPases of the Rho family, of which RND1 serves as a plexin activator yet its close homolog RhoD an inhibitor. Using molecular dynamics (MD) simulations we showed that RND1 reinforces plexin dimerization interface whereas RhoD destabilizes it due to their differential interaction with cell membrane. Upon binding plexin dimers at the Rho-GTPase binding (RBD) domains, RND1 and RhoD interact differently with the inner leaflet of cell membrane, and exert opposite effects on the dimerization interface via an allosteric network involving the RBD domain, RBD linkers, and a buttress segment adjacent to the dimerization interface. The differential membrane interaction is attributed to the fact that, unlike RND1, RhoD features a short C-terminal tail and a positively-charged membrane interface.
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