JOURNAL OF MEMBRANE SCIENCE
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2025
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IF 9
Yafei Cheng,Chen Wang,Miaomiao Zheng,Lan Yang,Lihai Fan,Longqiang Xiao,Xiaocheng Lin
Diffusion dialysis (DD) shows strong potential for acid reclamation, yet standard anion exchange membranes (AEMs) with compact, low-free-volume matrices impede ion transport, leading to low acid permeability and poor selectivity. To overcome these barriers, we present a new class of PIM-1-based AEMs fabricated through liquid bromine (Br 2 ) bromination followed by simultaneous crosslinking and cationization with 1,4-Diazabicyclo[2.2.2]octane (DABCO). This approach mitigates radical-induced chain scission, thereby better preserving the rigid polymer backbone while introducing a high density of ion-conducting sites with enhanced structural reinforcement. The resulting membranes exhibit interconnected micropores narrowly distributed at 0.4–0.6 nm, enabling molecular sieving between protons and multivalent cations. The optimized PIM-D/10h membrane achieves a proton dialysis coefficient of 37.0 × 10 −3 m/h and a separation factor (H + /Fe 2+ ) of 54.3, exceeding the commercial DF-120 benchmark by more than fourfold and threefold, respectively, while maintaining a tensile strength around 19 MPa and strong acid resistance. These results demonstrate that combining free-volume design with matrix reinforcement resolves the canonical permeability-selectivity compromise, thereby enabling a scalable route to durable AEMs for rapid, selective acid recovery from industrial wastewater.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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IF 8.5
Zheng Xing,Wenhao Yang,Chen Zhao,Yuhui Wang,Xiaolian Jiang,Song Qian,Yun Chu,Jiang Xia,Cheng Wang,Jianhao Wang
Androgenetic alopecia (AGA), the preeminent form of clinical hair loss, poses a significant challenge to patients. Growth factors (GFs) have been investigated for the treatment of hair loss. However, the issue of their optimal intra-dermal delivery remains a formidable obstacle. Type XVII collagen (COL17), which plays a crucial role in regulating the hair follicle aging process, has emerged as a highly promising candidate for hair loss treatment. Considering these constraints, we developed an I GF-1 loaded borate- m odified rh C OL 17 MN platform (I-mCOL17 MNs) for the treatment of AGA. The mCOL17 MNs are engineered to precisely control the release of bioactive payloads in response to dynamic changes in the microenvironment. A comprehensive investigation was conducted to verify the physicochemical characteristics, as well as the in vitro and in vivo biological activities of the MNs. Our findings demonstrate that, when contrasted with the clinically utilized drug minoxidil, our MN exhibits a remarkable capacity to enhance neovascularization, alleviate tissue-based inflammatory responses, and promote hair regeneration in murine models of AGA. Overall, this MN represents a novel, safer, and more efficient strategy for the treatment of AGA, offering new hope for patients suffering from this prevalent condition.
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JOURNAL OF RARE EARTHS
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2025
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IF 7.2
Xiaoshuai Zhang,Xi Wang,Tao Yin,Xuping Han,Panlai Li,Xiaoyan Yu,Zixuan Wang,Chengrun Liu,Zhijun Wang
The market demand for environmentally controlled agricultural indoor lighting is gradually increasing due to environmental pollution and drastic changes in the natural climate. Generally, matrix K 3 YSi 2 O 7 (phase 1) is difficult to synthesize compared to K 3 YSi 2 O 7 (phase 2), which has been illustrated by theoretical calculations. In this paper, large quantities of pure phase K 3 YSi 2 O 7 (phase 1) matrix were obtained by the substitution engineering strategy (Ca 2+ →Y 3+ ). Subsequently, Eu 2+ was doped to obtain a thermally stable ultra-wideband deep red light-emitting phosphor with an emission band centered at 721 nm and a full width at half maximum of 186 nm under 450 nm light excitation. It is noteworthy that compared with K 3 YSi 2 O 7 :Eu (phase 2), K 3 Ca 0.3 Y 0.7 Si 2 O 7 :Eu 2+ (phase 1) is superior in terms of emission wavelength, full width at half maximum, and thermal stability. Furthermore, the spectrum resemblance between its emission spectrum and the photosensitive pigment P fr was calculated to be 97.5%, which set the stage for subsequent plant lighting applications. Finally, light-emitting diode devices were prepared using K 3 Ca 0.3 Y 0.7 Si 2 O 7 :Eu 2+ phosphor for plant lighting experiments, and plants grown under deep red light emitting diode light show more luxuriant growth. The results show that the phosphor K 3 Ca 0.3 Y 0.7 Si 2 O 7 :Eu 2+ has promising applications in indoor plant culture. Meanwhile, the successful implementation of ion substitution engineering also provides a new strategy for transitions in host systems.
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Food Science & Nutrition
·
2024
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IF 3.5
Ruixi Luo,Yudie Hu,La Wang,Zunli Ke,Wenjia Wang,Ping Wang,Weiyi Tian
The primary catalyst for nonalcoholic fatty liver disease (NAFLD) is widely recognized as the induction of lipotoxicity in hepatocytes by an excess of fatty acids. In China, Penthorum chinense Pursh (PcP) is commonly employed as a functional food due to its known hepatoprotective properties. The present study aimed to investigate the influence of PcP extract on in vivo and in vitro models of NAFLD. We found that PcP extract can attenuate palmitic acid (PA)-induced lipotoxicity in HepG2 cells. PA was observed to trigger pyroptosis, as indicated by the increased expression of NLRP3 and GSDMD/N, activation of Caspase-1, and subsequent release of IL-1β and IL-18. However, these changes were reversed after PcP was administered. Furthermore, the application of an NLRP3 agonist inhibited the protective effects of PcP on lipotoxicity, indicating that PcP decreased lipotoxicity by inhibiting the NLRP3/Caspase-1/GSDMD pathway. Ultimately, we established a rat model of NAFLD through the administration of a high-fat diet (HFD), followed by the oral delivery of PcP extracts. The results demonstrated that the administration of PcP extract effectively decreased dyslipidemia and hepatic steatosis, which coincided with a decrease in hepatic pyroptosis through modulation of the NLRP3/Caspase-1/GSDMD pathway in liver tissues. Overall, our findings provide insight into the mechanism by which PcP extracts alleviate hepatic steatosis, highlighting the potential significance of modulating the NLRP3/Caspase-1/GSDMD pathway in the context of pyroptosis.
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Frontiers in Pharmacology
·
2025
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IF 4.8
Jinpeng Lv,Duo Meng,Huansha Zhang,Wenhui Xu,Xiaohong An,Chuanwei Yin,Kun Zou,Rongyin Gao
Introduction: Apigenin, a natural flavonoid with well-established antioxidant, anticancer, and anti-inflammatory activities, has recently attracted attention for its pigmentation-promoting effects. However, the underlying molecular mechanisms driving its melanogenic activity remain incompletely understood.Method: To investigate apigenin‘s effects on melanogenesis, human epidermal melanocytes (HEMCs), zebrafish embryos, and human skin explants were treated with apigenin. Melanin content, dendrite formation, and melanosome maturation were evaluated using spectrophotometry and transmission electron microscopy. Key signaling molecules and proteins involved in melanogenesis and melanosome transport were assessed by Western blotting and immunohistochemistry. The role of the c-KIT receptor was further explored through pharmacological inhibition and genetic knockdown approaches. Functional pigmentation was evaluated by assessing UVB-induced DNA damage markers.Results: Apigenin (10 μM) significantly increased melanin production by 1.8-fold in HEMCs, enhanced dendritic morphology, and promoted stage III–IV melanosome formation. Mechanistically, apigenin induced melanogenesis independently of the MC1R/cAMP/PKA pathway by directly binding to the c-KIT receptor, activating the Raf-1/ERK/RSK cascade, and upregulating MITF. This led to elevated expression of tyrosinase, TRP-1, TRP-2, and melanosome transport proteins Rab27a and Cdc42. Inhibition or knockdown of c-KIT abrogated these effects. In vivo, apigenin restored pigmentation in PTU-induced depigmented zebrafish and increased melanin content by 1.3-fold in human skin explants. Histological analysis confirmed effective melanin transfer to keratinocytes. Additionally, apigenin-treated skin showed reduced UVB-induced DNA damage, indicating enhanced photoprotection.Discussion: These findings demonstrate that apigenin stimulates melanogenesis through a novel c-KIT-dependent signaling pathway and promotes functional pigmentation with photoprotective benefits. Given its dietary origin, favorable safety profile, and multifaceted mechanisms, apigenin holds promise as a therapeutic agent for vitiligo and a natural pigmentation enhancer for dermatological use.
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BIORESOURCE TECHNOLOGY
·
2024
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IF 9.7
Xinyi Li,Tianbo Jia,Haiguang Zhu,Luhan Cai,Yubiao Lu,Jianxin Wang,Hengcong Tao,Peng Li
The CO 2 fixation mechanism by Alcaligenes faecalis ZS-1 in a biocathode microbial fuel cell (MFC) was investigated. The closed-circuit MFC (CM) exhibited a significantly higher CO 2 fixation rate (10.7%) compared to the open-circuit MFC (OC) (2.0%), indicating that bioelectricity enhances CO 2 capture efficiency. During the inward extracellular electron transfer (EET) process, riboflavin concentration increased in the supernatant while cytochrome levels decreased. Genome sequencing revealed diverse metabolic pathways for CO 2 fixation in strain ZS-1, with potential dominance of rTCA and C4 pathways under electrotrophic conditions as evidenced by significant upregulation of the ppc gene. Differential metabolite analysis using LC-MS demonstrated that CM promoted upregulation of various lipid metabolites. These findings collectively highlight that ZS-1 simultaneously generated electricity and fixed CO 2 and that the ppc associated with bioelectricity played a critical role in CO 2 capture. In conclusion, bioelectricity resulted in a significant enhancement in the efficiency of CO 2 fixation and lipid production.
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
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IF 4.8
Xi Ma,YuZheng Yang,Hao Li,ZeHong Luo,QiuYi Wang,XueMing Yao,Fang Tang,Ying Huang,Yi Ling,WuKai Ma
Although the pathogenesis of rheumatoid arthritis (RA) remains unclear, an increasing number of studies have confirmed that pyroptosis of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) is an important factor affecting the progression of RA. Periplogenin (PPN) is a natural cardiac glycoside; reportedly, it exerts anti-inflammatory and analgesic effects in diseases by inhibiting cell growth and migration. This study aimed to determine the effect of PPN on the growth, migration, and invasion of RA-FLS and the potential mechanism of pyroptosis regulation. We discovered that PPN could inhibit the migration and invasion abilities of RA-FLS and block their growth cycle, down-regulate the secretion and activation of NLRP3, Caspase-1, GSDMD, IL-1β, and IL-18, and reduce the number of pyroptosis. In summary, PPN inhibited pyroptosis, reduced the release of inflammatory factors, and improved RA-FLS inflammation by regulating the NLRP3/Caspase-1/GSDMD signaling pathway.
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SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY
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2024
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IF 4.3
Huan-Yu Sui,Dong Chen,Jia-Ping Huang,Zhe-Ying Hu,Lu Hu,Jie-Hua shi,Shao-Liang Jiang
Approval in 2019 was granted for the highly selective, targeted agent lorlatinib, which primary target is ROS1 and ALK. The purpose of this work was to examine the binding mechanism between lorlatinib (LOR) and HAG employing multispectral and molecular modeling techniques. Fluorescence data demonstrated that LOR quenched HAG fluorescence as a static quenching, interecalated into the hydrophobic cavity of HAG with a moderate affinity. Thermodynamic and competitive experiments pointed out that LOR bound with HAG primarily through hydrogen bonding, hydrophobic, and van der Waals forces. Circular dichroism, three-dimensional and synchronous fluorescence spectroscopic studies noted that the secondary structure of HAG and microenvironments around tyrosine (Tyr) and tryptophan (Trp) residues were altered due to binding with LOR. The contribution of each energy involved in binding process of LOR and HAG has been analyzed by molecular simulation techniques. Besides, the environmental conditions with metal ions have also been studied. The present study is expected to provide a theoretical basis for further studying the metabolism of LOR in vivo, which may help to gain a deeper understanding of the general pharmacological activity of the drug.
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EXPERIMENTAL CELL RESEARCH
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2021
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IF 3.905
Decai Chi,Dong Wang,Minghui Zhang,Hui Ma,Fuhui Chen,Yajiao Sun
Lung cancer is the leading cause of cancer mortality worldwide. CLEC12B , a C-type lectin-like receptor, is low-expressed in lung cancer tissues. However, the function of CLEC12B in lung cancer and its underlying mechanism remain unclear. Here, an obvious down-regulation of CLEC12B was observed in lung cancer cells compared with the normal lung epithelial cells. CLEC12B over-expression suppressed cell viability and cell cycle entry in lung cancer, along with the reduction of PCNA and cyclin D1 expressions, while silencing CLEC12B possessed the opposite effects. Over-expression of CLEC12B promoted lung cancer cell apoptosis, accompanied by decreased Bcl-2 and increased Bax, cleaved caspase-3 and cleaved caspase-9. Moreover, CLEC12B decreased phosphorylation of PI3K-p85 and AKT proteins. By contrast, CLEC12B knockdown activated the PI3K/AKT pathway. In vivo , CLEC12B inhibited tumor growth in lung cancer, which can be reversed by CLEC12B inhibition. Co-IP and immunofluorescence assays confirmed the interaction between CLEC12B and SHP-1, and CLEC12B over-expression increased SHP-1 level. Furthermore, knocking down SHP-1 abrogated the above biological phenotypes caused by CLEC12B elevation. Taken together, our findings demonstrate that CLEC12B serves as a tumor-suppressing gene in lung cancer through positively regulating SHP-1 expression, which may be mediated by the PI3K/AKT signaling pathway .
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Journal of Cancer
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2019
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IF 3.182
Huaizeng Chen,Jia Liu,Hanzhi Wang,Qi Cheng,Caiyun Zhou,Xiaojing Chen,Feng Ye
Background and Aims: Ovarian carcinoma (OC) is one of the most lethal malignant tumors with a high reoccurrence and chemoresistance. The key mechanism relationship with chemoresistance in ovarian carcinoma is still unclear. The existence of cancer stem cells involves in chemoresistance and reoccurrence in OC. The objective of this study was to investigate the expression, suppression of malignant properties and reversal of paclitaxel resistance inhibiting RNA-binding protein Musashi-1 with siRNA in ovarian cancer cells. Methods: The expression of MSI-1 was analyzed in 39 normal ovarian epithelia tissues, 92 serous cystadenomas, 68 borderline serous cystadenomas, and 97 serous cystadenocarcinomas by immunohistochemistry. pLKO.1-MSI-1-siRNA expression vector was transfected into ovarian carcinoma cell line A2780 and its paclitaxel-resistant cell subline A2780/Taxol. The roles of MSI-1 in proliferation, apoptosis, migration and invasion were explored by cell proliferation analysis, Caspase 3 activity assay, wound healing assay, migration and matrigel invasion assay, respectively. Western Blotting and Real-time quantitative PCR were conducted to detect the expression of MSI-1 and the ERK signaling pathway. Reversal of paclitaxel resistance assay was used to evaluate the role of MSI-1 in paclitaxel resistance of OC cells. Finally, therapeutic effects of MSI-1 inhibition were investigated the xenogratfs of SCID mice in vivo of the paclitacel-resistant. Results: MSI-1 is overexpressed and associated with an unfavorable prognosis in OC patients. Knockdown of MSI-1 by small interfering RNA (siRNA) inhibits proliferation, promotes apoptosis, and reduces migration and invasion of cancer cells. Moreover, MSI-1 expression inhibition reverses paclitaxel-resistance in OC cells. We further display that MSI-1 effectively protects OC cells from paclitaxel-induced apoptosis by increasing the expression of p-Bcl-2 through ERK signaling pathway activation. In vivo , MSI-1 siRNA clearly showed a strong effect on tumor growth inhibition and paclitaxel-resistance reversal. Conclusions: These findings suggest that MSI-1 overexpression is associated with the prognosis of OC patients, and knockdown of MSI-1 can suppress malignant properties and reverse paclitaxel-resistance in OC cells. MSI-1 maybe act as a potential prognostic indicator and a therapeutic target in OC.
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高影响因子
3 Biotech
·
2021
·Vol. 11
·期 12
·1-13
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IF 2.406
Tang Miaolong,Cai Jimin,Wang Yan,Huan Zhirong,Yao Hao,Xu Ce,Ge Xin,Song Sheng
Hemorrhage shock (HS) is a major threat to patients with trauma and spontaneous bleeding, resulting in multi-organ failure including the kidney. Tyrosine kinase nonreceptor 1 (TNK1) has been shown to be upregulated in the kidney of experimental HS and patients with severe trauma . The study aims to investigate the role of TNK1 and the underlying mechanism in HS-induced kidney injury. A model of HS was established with femoral artery bloodletting, followed by resuscitation in Sprague–Dawley rats. Renal expression of TNK1 was abnormally induced by HS in rats. Knockdown of TNK1 alleviated HS-induced cell apoptosis and the level of proinflammatory cytokines (TNF-α, IL-6 and IL-1β) in the kidney. The expression of M1 macrophage markers (CD86 and iNOS) and the activation of STAT1 were inhibited by TNK1 knockdown in HS rats. In vitro, human monocyte THP-1 cells were treated with 20 ng/mL interferon-gamma plus 100 ng/mL lipopolysaccharide to induce M1 polarization. TNK1 knockdown exerted inhibitory effect on macrophage M1 polarization, M1-type inflammatory cytokine production and STAT1 activation in THP-1 cells. In conclusion, downregulation of TNK1 alleviates HS-induced kidney injury by suppressing macrophage M1 polarization, inflammation and kidney cell apoptosis, in which the deactivation of STAT1 signaling may be involved.
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Frontiers in Pharmacology
·
2022
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IF 5.988
Li Dafei,Zhao Haiyan,Xu Piao,Lin Qiongping,Zhao Tingting,Li Chubing,Cui Zhong-Kai,Tian Guangyong
Irreversible sensorineural hearing loss is one of the most common side effects after cisplatin treatment. Prevention and reversal of hearing loss caused by cisplatin are of great importance for cancer patients, especially children. Oxidative stress is an important cause of hearing loss resulted from cisplatin, unfortunately, there is no drug yet available that can completely prevent and reverse the ototoxicity from cisplatin. Polydatin (PD) possesses excellent antioxidant and anti-inflammatory effects, however, its role in the cisplatin-induced hearing loss has not been investigated. Herein, we have explored the preventive and therapeutic effects of PD on cisplatin-induced hearing loss and the possible underlying mechanisms. In the in vivo setting with guinea pigs, we have demonstrated that PD can reduce the threshold shift of auditory brainstem response (ABR) caused by cisplatin, promote the nuclear translocation of Nuclear factor erythroid-2 related factor 2 (Nrf2), increase the expression of Nrf2 and heme oxygenase-1 (HO-1), and thus reduce the loss of outer hair cells (OHCs). PD can ameliorate cisplatin-induced hearing loss through activating the Nrf2/HO-1 signaling pathway. This study provides a potential strategy for preventing and improving hearing loss resulted from cisplatin treatment in clinics.
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