：Background: The frequency of take-out food consumption has increased rapidly among Chinese college students, which has contributed to high obesity prevalence. However, the relationships between take-out food consumption, body mass index (BMI), and other individual factors influencing eating behavior among college students are still unclear. This study explored the association of take-out food consumption with gender, BMI, physical activity, preference for high-fat and high-sugar (HFHS) food, major category, and degree level among Chinese college students. Methods: Cross-sectional data were collected from 1220 college students in Beijing, China, regarding information about take-out food consumption, physical activity, and preference for HFHS food using a self-reported questionnaire. The logistic linear regression model was used to analyze the association between take-out food consumption and personal and lifestyle characteristics. Results: Out of 1220 college students, 11.6% of college students were overweight or obese. Among the personal and lifestyle characteristics, high frequency of take-out food consumption was significantly associated with a non-medical major, high preference for HFHS food, degree level, and higher BMI, but not physical activity. Conclusion: Among Chinese college students, consumption of take-out food may be affected by major category, preference for HFHS food, degree level, and BMI. This could provide guidance on restrictions of high take-out food consumption, which contributes to high obesity prevalence and high risk for metabolic diseases.

Parkinson's disease (PD) is a chronic neurodegenerative disorder that is characterized by motor symptoms as a result of a loss of dopaminergic neurons in the substantia nigra pars compacta (SNc), accompanied by chronic neuroinflammation, oxidative stress, formation of α-synuclein aggregates. Celastrol, a potent anti-inflammatory and anti-oxidative pentacyclic triterpene, has emerged as a neuroprotective agent. However, the mechanisms by which celastrol is neuroprotective in PD remain elusive. Here we show that celastrol protects against dopamine neuron loss, mitigates neuroinflammation, and relieves motor deficits in MPTP-induced PD mouse model and AAV-mediated human α-synuclein overexpression PD model. Whole-genome deep sequencing analysis revealed that Nrf2, NLRP3 and caspase-1 in SNc may be associated with the neuroprotective actions of celastrol in PD. By using multiple genetically modified mice (Nrf2-KO, NLRP3-KO and Caspase-1-KO), we identified that celastrol inhibits NLRP3 inflammasome activation, relieves motor deficits and nigrostriatal dopaminergic degeneration through Nrf2-NLRP3-caspase-1 pathway. Taken together, these findings suggest that Nrf2-NLRP3-caspase-1 axis may serve as a key target of celastrol in PD treatment, and highlight the favorable properties of celastrol for neuroprotection, making celastrol as a promising disease-modifying agent for PD.

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The pathogenesis of Parkinson’s disease (PD) remains unclear, and there is no disease-modifying agent for PD. Withaferin A (WA), a naturally occurring compound, has emerged as a neuroprotective agent. However, the mechanisms by which WA is neuroprotective in PD are unknown. Here we show that WA protected against loss of dopaminergic neurons, neuroinflammation, and motor deficits in MPTP-induced PD mouse models. Whole-genome deep sequencing analysis combined with Meta-analysis of human PD studies reveal that DJ1, Nrf2, and STING in substantia nigra pars compacta (SNc) are linked to anti-PD effect of WA. We found that WA activated DJ1 and Nrf2, and suppressed STING within SNc; and overexpression of STING in SNc dampened the effect of WA. Using genetically modified mice (DJ1-KO, Nrf2-KO, STINGgt/gt and STING-KO) and immunolabeling technique, we identified that WA targeted DJ1-Nrf2-STING pathway in dopaminergic neurons; and we demonstrate that STING might be an important factor in PD pathogenesis. In addition, WA alleviated accumulation of phosphorylated α-synuclein (p-α-syn) and insoluble α-syn within SNc in adeno-associated virus (AAV)-mediated human α-syn overexpression PD model. Our comparative analysis on whole-genome transcriptome profiles suggests that STING might be a key target of WA and amantadine in PD treatment. This study highlights a multifaceted role for WA in neuroprotection, and suggests that WA can be a potential candidate for treatment of PD.

Celastrol prevents high-fat diet-induced obesity by promoting white adipose tissue browningDear Editor, Despite advances in therapy for obesity, effective therapeutic strategies for weight loss are still needed. 1 Our team revealed that celastrol promoted white adipose tissue (WAT) browning, and protected against high-fat diet (HFD)-induced obesity via activation of hypothalamussympathetic nervous system -β 3 AR axis. Fatty acid transport 2 (Fatp2) may serve as an important factor to mediate the browning-inducing effects of celastrol. This study may provide a basis for exploring a new strategy for the treatment of obesity.Celastrol is a leptin sensitizer. 2 We found that long-term treatment with celastrol at doses of 10 and 1 μg/kg prevented the development of obesity (Figure S1A,B). Food intake was suppressed by celastrol at dosages of 1000, 100 and 10 μg/kg, but not 1 μg/kg (Figure S1C,D). Celastrol treatment at doses of 1000 and 100 μg/kg resulted in a severe decline in food intake and body weight in HFDfed mice by 4-5 days (Figure S1A-C). Increased UCP1 expression was observed in inguinal WAT (iWAT) of the mice treated with celastrol at a dose of 1 μg/kg (Figure S1E). The canonical molecular and morphological characteristics of WAT browning including the increased protein levels of uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor-UCP1 and PGC1γ coactivator 1-α (PGC1α), and the decreased size of multilocular adipocytes were also seen in iWAT (Figure S1F-H). The increased expressions of WAT browning-associated genes were not seen in mice treated with celastrol at a dose of .1 μg/kg (Figure S1I). The HFD-induced obesity was prevented by celastrol at the dose of 1 μg/kg during a 3-month treatment without affecting food intake (Figure 1A-E). A sustained expression of WAT browningassociated genes was observed in iWAT of celastrol-treated mice (Figure 1F). Celastrol diminished the increment of adiposity in both room temperature (RT) and thermoneutrality (Figure 1G-I,K). No significant difference in the food intake was found (Figure 1J). Celastrol stimulated expressions of WAT browning-associated genes in iWAT atThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.