Perfluorooctane sulfonate aggravates CCl4-induced hepatic fibrosis via HMGB1/TLR4/Smad signaling.

Perfluorooctane sulfonate (PFOS) is a widespread environmental pollutant and may cause a variety of adverse health effects. The hepatotoxicity of PFOS has attracted particular attention, given the fact that the liver has one of the highest PFOS accumulations among human tissues. In this study, we revealed that subchronic PFOS exposure may exacerbate carbon tetrachloride (CCl )-induced liver fibrosis in animal models.

PFOS facilitates liver inflammation and steatosis: An involvement of NLRP3 inflammasome-mediated hepatocyte pyroptosis.

Perfluorooctane sulfonate (PFOS) is a fluorinated organic pollutant with substantial accumulation in mammalian liver tissues. However, the impact of chronic PFOS exposure on liver disease progression and the underlying molecular mechanisms remain elusive. Herein, we for the first time revealed that micromolar range of PFOS exposure initiates the activation of NLR pyrin domain containing 3 (NLRP3) inflammasome to drive hepatocyte pyroptosis.

Nicotine triggers islet β cell senescence to facilitate the progression of type 2 diabetes.

Cigarette smoking is a well-recognized risk factor for type 2 diabetes (T2DM), and may result in islet β cell damage and impaired insulin secretion. However, the underlying mechanisms remain largely elusive. In the present study, we demonstrated that nicotine induced premature senescence of pancreatic β cells in vitro and in vivo.

ROS-mediated JNK pathway critically contributes to PFOS-triggered apoptosis in SH-SY5Y cells.

Recent studies have indicated that perfluorooctane sulfonate (PFOS) and its derivatives can lead to neurotoxicity. In the present study, we showed that PFOS may trigger neuronal apoptosis through a c-Jun N-terminal kinase (JNK)-related mechanism. We revealed that c-Jun N-terminal kinase (JNK) was robustly activated in PFOS-exposed neuronal cells.

Ring roads and urban biodiversity: distribution of butterflies in urban parks in Beijing city and correlations with other indicator species.

The capital of China, Beijing, has a history of more than 800 years of urbanization, representing a unique site for studies of urban ecology. Urbanization can severely impact butterfly communities, yet there have been no reports of the species richness and distribution of butterflies in urban parks in Beijing. Here, we conducted the first butterfly survey in ten urban parks in Beijing and estimated butterfly species richness.

Nrf2 Signaling Elicits a Neuroprotective Role Against PFOS-mediated Oxidative Damage and Apoptosis.

Perfluorooctanesulfonate (PFOS) may cause neurotoxicity through the initiation of oxidative stress. In the current study, we investigated the role of anti-oxidant nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in PFOS-induced neurotoxicity. We found that human neuroblastoma SH-SY5Y cells exhibited significant apoptotic cell death following PFOS exposure, and this process was accompanied with apparent accumulation of reactive oxidative species (ROS).

Perfluorooctane sulfonate mediates secretion of IL-1β through PI3K/AKT NF-кB pathway in astrocytes.

Perfluorooctane sulfonate (PFOS) is a persistent and bioaccumulative compound that has been widely used in various fields of life and industrial productions, because of its special chemical and physical properties. Numerous studies have indicated significant neurotoxic effect of PFOS, especially on neurons and microglia. However, the influence of PFOS on astrocyte physiology remains unclear.