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SEPARATION AND PURIFICATION TECHNOLOGY · 2023 · IF 8.6

The overlooked role of the association between 2-methylisoborneol and natural organic matters in the nanofiltration treatment of authentic water

Hui Yang,Lei Li,Junyi Li,Shuili Yu,Naiyun Gao,Charles Flomo Togbah

The presence of natural organic matter (NOM) in surface water and its significance for removing pollutants during nanofiltration (NF) are overlooked since most previous studies were conducted in synthetic water rather than real water. In this paper, using raw water collected from Lake Tai (the third largest lake in China), we investigate the removal of 2-methylisoborneol (2-MIB, one of the most concerned off-flavor compounds in raw water) by NF and analyze the binding behaviors between 2-MIB and NOM, which affect their corresponding migration and removal behaviors of 2-MIB during NF. The results show that the removal of 2-MIB in real raw water is 12.2 ∼ 22.0 % higher than that in pure water (PW). Additionally, we evaluate the increment of the removal of 2-MIB under different backgrounds, which follow the order NOM (17.2 %∼22.0 %) > bovine serum albumin (BSA 16.0 %∼19.1 %) > intracellular organic matter (IOM) of M. aeruginosa (8.3 %∼9.4 %) > sodium carboxymethyl cellulose (CMC 3.9 %∼6.5 %) > humic acid (HA 0.28 %∼0.31 %). These findings demonstrate that the protein-like components in raw water play a major role in binding to 2-MIB, while humic-like components exhibit a weak association with 2-MIB. Overall, the conclusion and findings in this study provide a new perspective on the NOM effect on micropollutant removal during water treatment.

CAS / MDL: 7647-14-5 67-56-1
研究领域: 环境科学 · 水处理工程
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ACS Applied Materials & Interfaces · 2024 · IF 8.3

Bioinspired Sulfobetaine Borneol Fluorinated Amphiphilic Polymers for Marine Antifouling and Fouling Release Applications

Zhongqiang Yu,Wen Sun,Lida Wang,Zhengqing Yang,Yine Ren,Yanke Li,Guichang Liu,Qian Zhang

The development of nontoxic antifouling coatings in static marine environments is urgent. Herein, the successful synthesis of sulfobetaine borneol fluorinated polymers (PEASBF) by a free radical polymerization method is reported. The PEASBF coatings exhibit outstanding antifouling activity, which effectively resists the adhesion of Bovine serum albumin (FITC-BSA adhesion rate: 0.5%), Pseudomonas sp. (Biofilm: 1.3 absorbance) and Navicula sp. (Diatom attachment rate: 33%). More importantly, the PEASBF coatings display outstanding fouling release properties, achieving a release rate of 98% for Navicula sp., and the absorbance of the Pseudomonas sp. biofilm is only 0.2 under 10 Pa shear stress. XPS and MD studies showed that the fluorinated/isobornyl groups induce more sulfobetaine groups to migrate toward polymer surfaces for intensify antifouling. Additionally, the chiral stereochemical structure of borneol enhances antifouling and fouling release ability of amphiphilic polymers. Therefore, the PEASBF has the potential for static marine antifouling applications.

研究领域: 材料科学 · 海洋生物学
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TOXICOLOGY AND APPLIED PHARMACOLOGY · 2025 · IF 3.4

S100A11 mediates the protective effects of edaravone dexborneol on docetaxel-induced cognitive impairment in rats by inhibiting the MAPK signaling pathway

Ping Liu,Jiantao Jia,Yinliang Lu,Hanmin Tang,Chengyi Gao,Suxia Han

Cognitive impairment is a common side effect of docetaxel (DTX)-based chemotherapy. The novel neuroprotective agent edaravone dexborneol (ED) was found to alleviate the adverse phenotype caused by DTX. However, the underlying mechanism remains unexplored. By analyzing mRNA-sequencing data, we noticed that the expression of S100 calcium-binding protein A11 (S100A11), a protector of the nervous system, was decreased in DTX-treated rats with cognitive damage, but ED administration reversed the trend. Therefore, we speculated that S100A11 might be involved in the protective effects of ED on DTX-induced cognitive impairment. Sprague-Dawley rats were intraperitoneally injected with DTX to induce cognitive impairment, followed by intraperitoneal injection of ED after DTX induction. The results showed that ED treatment mitigated cognitive impairment caused by DTX. Next, adenoviruses carrying sequences encoding S100A11 were given to rats receiving DTX treatment. S100A11 overexpression alleviated cognitive dysfunction of DTX-treated rats, as evidenced by the decreased escape latency and swimming distance, and the increased number of platform crossings. Mechanically, S100A11 overexpression inhibited neuronal apoptosis by inactivating the MAPK signaling pathway. Further rescue experiments showed that S100A11 knockdown reversed the defensive role of ED in DTX-induced neuronal damage. In conclusion, ED ameliorates cognitive dysfunction caused by DTX by upregulating the S100A11 expression and subsequently inactivating the MAPK signaling pathway.

CAS / MDL: 28718-90-3
研究领域: 神经科学 · 药理学 · 分子生物学 · 肿瘤学 · 生物化学
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EUROPEAN JOURNAL OF PHARMACOLOGY · 2023 · IF 5

Edaravone dexborneol ameliorates cognitive impairment by regulating the NF-κB pathway through AHR and promoting microglial polarization towards the M2 phenotype in mice with bilateral carotid artery stenosis (BCAS)

Lei Li,Guojun He,Mingyu Shi,Juehua Zhu,Yongqing Cheng,Yang Chen,Jin Chen,Qun Xue

Cerebral small vessel disease (CSVD) is one of the most important causes of stroke and vascular dementia , so exploring effective treatment modalities for CSVD is warranted. This study aimed to explore the anti-inflammatory effects of Edaravone dexborneol (C.EDA) in a CSVD model. Mice with CSVD showed distinct cognitive decline, as assessed by the Morris water maze (MWM). Pathological staining verified leakage across the blood‒brain barrier (BBB), microglial proliferation, neuronal loss and demyelination . Western blot analysis demonstrated that M1 microglia dominated prophase and released proinflammatory molecules; the aryl hydrocarbon receptor (AHR) was found to participate in modulating nuclear factor-kappa B (NF-κB) signalling activation through tumour necrosis factor receptor-associated factor-6 (TRAF6). C.EDA treatment resulted in the polarization of microglia from the M1 to the M2 phenotype. Mice sequentially treated with C.EDA exhibited a significant improvement in cognitive function; expression of the anti-inflammatory cytokines and modulatory proteins AHR and TRAF6 was upregulated, while the levels of pNF-κBp65 and pIΚBα were downregulated. C.EDA promoted microglial activation towards the M2 phenotype by upregulating AHR expression, which prevented TRAF6 ubiquitination , promoted NF-κB RelA/p65 protein degradation and inhibited subsequent NF-κB phosphorylation. Mechanistically, the anti-inflammatory effect of C.EDA alleviated neuronal loss and myelin damage, while at the functional level, C.EDA improved cognitive function and thus showed good application prospects.

CAS / MDL: 57-55-6
研究领域: 神经科学 · 药理学 · 神经退行性疾病 · 炎症
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