Mitochondrial dysregulation has been implicated in oxidative stress-induced melanocyte destruction in vitiligo. However, the molecular mechanism underlying this process is merely investigated. Given the prominent role of nicotinamide adenine dinucleotide (NAD + )-dependent deacetylase Sirtuin3 (SIRT3) in sustaining mitochondrial dynamics and homeostasis and that SIRT3 expression and activity can be influenced by oxidative stress-related signaling, we wondered whether SIRT3 could play an important role in vitiligo melanocyte degeneration by regulating mitochondrial dynamics. Methods: We initially testified SIRT3 expression and activity in normal and vitiligo melanocytes via PCR, immunoblotting and immunofluorescence assays. Then, cell apoptosis, mitochondrial function and mitochondrial dynamics after SIRT3 intervention were analyzed by flow cytometry, immunoblotting, confocal laser microscopy, transmission electron microscopy and oxphos activity assays. Chromatin immunoprecipitation (ChIP), co-immunoprecipitation (Co-IP), immunoblotting and immunofluorescence assays were performed to clarify the upstream regulatory mechanism of SIRT3. Finally, the effect of honokiol on protecting melanocytes and the underlying mechanism were investigated via flow cytometry and immunoblotting analysis. Results: We first found that the expression and the activity of SIRT3 were significantly impaired in vitiligo melanocytes both in vitro and in vivo . Then, SIRT3 deficiency led to more melanocyte apoptosis by inducing severe mitochondrial dysfunction and cytochrome c release to cytoplasm, with Optic atrophy 1 (OPA1)-mediated mitochondrial dynamics remodeling involved in. Moreover, potentiated carbonylation and dampened peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) activation accounted for SIRT3 dysregulation in vitiligo melanocytes. Finally, we proved that honokiol could prevent melanocyte apoptosis under oxidative stress by activating SIRT3-OPA1 axis. Conclusions: Overall, we demonstrate that SIRT3-dependent mitochondrial dynamics remodeling contributes to oxidative stress-induced melanocyte degeneration in vitiligo, and honokiol is promising in preventing oxidative stress-induced vitiligo melanocyte apoptosis.

Mood disorders have multiple phenotypes and complex underlying biological mechanisms and, as such, there are no effective therapeutic strategies. A review of recent work on the role of astrocytes in mood disorders is thus warranted, which we embark on here. We argue that there is tremendous potential for novel strategies for therapeutic interventions based on the role of astrocytes. Astrocytes are traditionally considered to have supporting roles within the brain, yet emerging evidence has shown that astrocytes have more direct roles in influencing brain function. Notably, evidence from postmortem human brain tissues has highlighted changes in glial cell morphology, density and astrocyte-related biomarkers and genes following mood disorders, indicating astrocyte involvement in mood disorders. Findings from animal models strongly imply that astrocytes not only change astrocyte morphology and physiological characteristics but also influence neural circuits via synapse structure and formation. This review pays particular attention to interactions between astrocytes and neurons and argues that astrocyte dysfunction affects the monoaminergic system, excitatory–inhibitory balance and neurotrophic states of local networks. Together, these studies provide a foundation of knowledge about the exact role of astrocytes in mood disorders. Importantly, we then change the focus from neurons to glial cells and the interactions between the two, so that we can understand newly proposed mechanisms underlying mood disorders, and to identify more diagnostic indicators or effective targets for treatment of these diseases.

The isoquinoline plant alkaloid berberine has anti-tumor effects on a variety of carcinoma cells, mainly through inhibition of cell proliferation, apoptosis induction and cell cycle arrest. However, the mechanisms underlying its role in tumor progression are unknown. In the present study, we investigated the molecular mechanisms involved in berberine-induced cell death in human hepatoma carcinoma cell (HCC) lines HepG2 and SMMC7721. Our results showed that berberine inhibited tumor cell viability in a dose-and time-dependent manner, and induced cell death via apoptosis and autophagy. Moreover, berberine treatment significantly inhibited CD147 expression by HCC cells in a dosedependent manner. Overexpression of CD147 protein markedly reduced berberine-induced cell death. Our data provide the first experimental evidence that berberine induces cell death in HCC cells via downregulation of CD147 and suggest a new mechanism to explain its anti-tumor effects. (Cancer Sci 2011; 102: 1287-1292 B erberine is an isoquinoline alkaloid found in a number of important medicinal plant species such as Berberis aristata and Berberis aquifolium, and has antibacterial,(1) anti-hypertensive, (2) anti-inflammatory, (3) anti-diabetic (4) and anti-hyperlipidemic effects.(5) Recently, researchers have become interested in the anti-neoplastic activities of berberine and have demonstrated its anticancer effects against a variety of human cancer cells both in vitro and in vivo through suppression of tumor cell proliferation, induction of tumor cell apoptosis, and inhibition of both tumor invasion and metastasis.(6,7) These findings suggest that berberine is a promising candidate for clinical use in cancer chemotherapy.Hepatocellular carcinoma (HCC) is the sixth most common malignancy worldwide and the third leading cause of death from cancer because of its very poor prognosis. More than 1 million cases of HCC occur in the world each year.(8) Hepatocellular carcinoma is highly resistant to conventional systemic therapies and the prognosis for patients with advanced HCC remains poor. Although a lot of progress has been made in terms of chemotherapy, which provides significant survival benefits for patients with HCC, it is associated with significant side-effects, highlighting the need for therapeutic strategies that target tumor cells without compromising normal tissue function.(9,10) Thus, the development of novel systemic agents from natural products with low toxicity and few side-effects is being actively pursued. (11)(12)(13) Previous studies confirm the anti-tumor effects of berberine on HCC. (14)(15)(16) Berberine acts by inhibiting proliferation and inducing apoptosis in HCC cells. It can also inhibit the migration of HCC cells by downregulating the Rho ⁄ ROCK signaling pathway.(17) However, the exact mechanisms underlying the anti-tumor effects of berberine are still unknown. CD147, a glycosylated immunoglobulin super family transmembrane protein, is highly expressed by HCC cells. Several in vitro studies suggest that CD147 promotes...

Abstract. Currently, the emission inventory of vehicular volatile organic compounds (VOCs) is one of those with the largest errors and uncertainties due to suboptimal estimation methods and the lack of first-hand basic data. In this study, an updated speciated emission inventory of VOCs and an estimation of intermediate-volatility organic compounds (IVOCs) from vehicles in China at the provincial level for the year of 2015 are developed based on a set of state-of-the-art methods and an abundance of local measurement data. Activity data for light-duty vehicles are derived from trajectories of more than 70 000 cars for 1 year. The annual mileage of trucks are calculated from reported data by more than 2 million trucks in China. The emission profiles are updated using measurement data. Vehicular tailpipe emissions (VTEs) and four types of vehicular evaporation emissions (VEEs), including refueling, hot soak, diurnal and running loss, are taken into account. Results show that the total vehicular VOC emissions in China are 4.21 Tg (with a 95 % confidence interval range from 2.90 to 6.54 Tg) and the IVOC emissions are 200.37 Gg in 2015. VTEs are still the predominant contributor, while VEEs are responsible for 39.20 % of VOC emissions. The control of VEEs is yet to be optimized in China. Among VTEs, passenger vehicles emissions have the largest share (49.86 %), followed by trucks (28.15 %) and motorcycles (21.99 %). Among VEEs, running loss is the largest contributor (81.05 %). For both VTEs and VEEs, Guangdong, Shandong and Jiangsu province are three of the highest, with a respective contribution of 10.66, 8.85 and 6.54 % to the total amounts of VOCs from vehicles. 97 VOC species are analyzed in this VOC emission inventory. i-Pentane, toluene and formaldehyde are found to be the most abundant species in China's vehicular VOC emissions. The estimated IVOCs are another "inconvenient truth", concluding that precursor emissions for secondary organic aerosol (SOA) from vehicles are much larger than previously estimated.

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Abstract. Emissions from ships at berth play an important role regarding the exposure of high density human populations to atmospheric pollutants in port areas; however, these emissions are not well understood. In this study, volatile organic compounds (VOCs) and particle emissions from 20 container ships at berth were sampled and analyzed during the "fuel switch" period at Jingtang Port in Hebei Province, China. VOCs and particles were analyzed using a gas chromatography-mass spectrometer (GC-MS) and a single particle aerosol mass spectrometer (SPAMS), respectively. VOC analysis showed that alkanes and aromatics, especially benzene, toluene and heavier compounds e.g., n-heptane, noctane and n-nonane, dominated the total identified species. Secondary organic aerosol (SOA) yields and ozone (O 3 ) forming potential were 0.017 ± 0.007 g SOA g −1 VOCs and 2.63 ± 0.37 g O 3 g −1 VOCs, respectively. Both positive and negative ion mass spectra from individual ships were derived and the intensity of specific ions were quantified. Results showed that elemental carbon (35.74 %), elemental carbon-organic carbon mixtures (33.95 %) and Na-rich particles (21.12 %) were major classes, comprising 90.7 % of the particles observed. Particles from ship auxiliary engines were in the 0.2 to 2.5 µm size range, with a peak occurring at around 0.4 µm. The issue of using vanadium (V) as tracer element was examined, and it was found that V was not a proper tracer of ship emissions when using low sulfur content diesel oil. The average percentage of sulfate particles observed in shipping emissions before and after switching to marine diesel oil remained unchanged at 24 %. Under certain wind conditions, when berths were upwind of emission sources, the ratios before and after 1 January were 35 and 27 % respectively. The impact of atmospheric stability was discussed based on PM 2.5 and primary pollutant (carbon monoxide) concentration. With a background of frequent haze episodes and complex mechanisms of particulate accumulation and secondary formation, the impact of atmospheric stability is believed to have been weak on the sulfate contribution from shipping emissions. The results from this study provide robust support for port area air quality assessment and source apportionment.

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