Chirality is not only a natural phenomenon but also a bridge between chemistry and life sciences. An effective way to obtain a single enantiomer is through racemates resolution. Recent literature shows that chiral metal-organic frameworks (CMOFs) have many applications in various fields because of their diverse topologies and functionalities. This review outlines the design idea and summarizes the latest synthesis strategies and applications of CMOFs. It highlights key advances and issues in the separation domain. In conclusion, the review provides perspectives on the challenges and prospective advancements of CMOFs materials and CMOFs-based separation technologies.

Chirality is not only a natural phenomenon but also a bridge between chemistry and life sciences.An effective way to obtain a single enantiomer is through racemates resolution.Recent literature shows that chiral metal-organic frameworks(CMOFs)have many applications in various fields because of their diverse topologies and functionalities.This review outlines the design idea and summarizes the latest synthesis strategies and applications of CMOFs.It highlights key advances and issues in the separation domain.In conclusion,the review provides perspectives on the challenges and prospective advance-ments of CMOFs materials and CMOFs-based separation technologies.

Objective To investigate the protective effect of resveratrol on intestinal barrier in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced Parkinson's disease(PD)mouse models and its mechanism for regulating TLR4/MyD88/NF-κB signaling to protect dopaminergic neurons.Methods Fifty-two C57BL/6J mice were randomized into control group(n= 12),MPTP group(n=14),MPTP+resveratrol(30 mg/kg)group(n=13),and MPTP+resveratrol(90 mg/kg)group(n=13),and mouse models were established by intraperitoneal MPTP(30 mg/kg)injection for 7 days in the latter 3 groups.Behavioral tests were conducted to evaluate the effect of resveratrol on motor symptoms of the mice.Western blotting was used to detect the expression of TH,α-syn,ZO-1,Claudin-1,TLR4,MyD88,and NF-κB in the brain tissues of the mice.Immunohistochemistry,immunofluorescence,ELISA and transmission electron microscopy were used to verify the effect of resveratrol for suppressing inflammation and protecting the intestinal barrier.Results Compared with those in the normal control group,the mice in MPTP group showed significant changes in motor function,number of dopaminergic neurons,neuroinflammation,levels of LPS and LBP,and expressions of tight junction proteins in the intestinal barrier.Resveratrol treatment significantly improved motor function of the PD mice(P<0.01),increased the number of neurons and TH protein expression(P<0.05),down-regulated the expressions of GFAP,Iba-1,and TLR4,lowered fecal and plasma levels of LPS and LBP(P<0.05),restored the expression levels of ZO-1 and Claudin-1(P<0.01),and down-regulated the expressions of TLR4,MyD88,and NF-κB in the colon tissue(P<0.05).The mice with resveratrol treatment at 30 mg/kg showed normal morphology of the tight junction complex with neatly and tightly arranged intestinal villi.Conclusion Resveratrol repairs the intestinal barrier by inhibiting TLR4/MyD88/NF-κB signaling pathway-mediated inflammatory response,thereby improving motor function and neuropathy in mouse models of MPTP-induced PD.

Objective: To understand the relationship between serum 25 hydroxyvitamin D [25(OH)D] levels and social emotional functions in children with autism spectrum disorder (ASD), in order to provide the reference for comprehensive interventions in ASD children. Methods: From January to June 2024, 124 ASD children aged 1-3 who received rehabilitation training at designated rehabilitation institutions in Nantong City, China were selected as the case group, while 124 healthy gender and age matched children who underwent health examinations at the same time were selected as the control group. The study used liquid chromatography-mass spectrometry to measure serum 25(OH)D levels in both groups of children. The Chinese Infant-Toddler Social and Emotional Assessment (CITSEA) was used to evaluate the emotional and socialization functioning of children with ASD, and to explore the relationship between serum 25(OH)D levels and their emotional and social functioning. Results: The serum 25(OH)D levels were lower in the case group [(59.22±19.96)nmol/L] compared to the control group [(85.50±21.59)nmol/L], and the rate of 25(OH)D deficiency or insufficiency (21.77%) was higher than that of the control group (7.26%), with statistically significant differences ( t/χ 2=-7.75, 8.91, P <0.01). The CITSEA evaluation results showed that the scores of the explicit behavior domain, implicit behavior domain, dysregulation domain, and ability domain in children with ASD were (63.37±10.44, 56.29± 9.36 , 57.04±10.65, 38.92±17.91) points, and the abnormal detection rates were 50.81%, 35.48%, 41.13%, and 45.16%, respectively. Among them, the abnormal detection rates of the explicit behavior domain and ability domain were higher in boys ( 57.14 %, 51.02%) compared to girls (34.62%, 23.08%), and the differences were statistically significant ( χ 2=4.18, 6.48, P < 0.05 ). The abnormal detection rates of explicit behavioral domains and dysregulated domains in ASD children with insufficient or deficient serum 25(OH)D (77.78%, 59.26%) were higher than those in the normal serum 25(OH)D group (37.11%, 18.56%), and the differences were statistically significant ( χ 2=14.06, 17.58, P <0.01). Conclusion The serum 25(OH)D levels in children with ASD are significantly lower compared to levels in healthy children, and developmental abnormalities in social emotional functioning are common concurrent problems.

OBJECTIVE To investigate the effect of Banxia Xiexin decoction(BXD) on colitis associated cancer(CAC) mice and its related mechanism. METHODS Seventy-five C57BL/6 mice were randomly divided into normal group, model group, Banxia Xiexin decoction low-dose group, high-dose group and mesalazine group. Except for the normal group, the mice in the other groups were intraperitoneally injected with azoxymethane combined with oral dextran sodium sulfate to establish the CAC model. BXD and mesalazine were given respectively for intervention. The general conditions of all mice were observed and recorded, and the changes of body weight, disease activity index, colon length and tumor number were monitored. HE staining was utilized to observe the pathological changes of colon tissue. The expression levels of PCNA, NF-κB P65 and IκB-α were detected by immunohistochemistry. The mRNA levels of IL-17A, N-cadherin, E-cadherin and Bcl-2 were detected by qRT-PCR. Macrophage infiltration was measured using immunostaining analysis. Western blotting was applied to analyze the expression of NF-κB, E-cadherin and N-cadherin proteins in colon tissues of each group. RESULTS There was no significant tumor occurrence in the normal group, while the body weight of the model group mice was significantly reduced and the number of colon tumors increased. The colon length, number of tumors, and degree of inflammatory cell infiltration in the BXD group were significantly improved compared to the model group. Immunohistochemical results showed that the expression of PCNA, NF-κB P65 and IκB-α protein in colon tissue of model group was remarkably increased (P<0.01). Immunofluorescence results showed that the number of F4/80, CD80 and CD206 positive macrophages in the colon tissue of the model group increased (P<0.05 or P<0.01). The results of RT-PCR demonstrated that the levels of IL-17A, N-cadherin and Bcl-2 mRNA in the colon tissue of the model group were significantly increased (P<0.01), while the level of E-cadherin mRNA was fundamentally decreased (P<0.01). Western blotting results displayed that the expression levels of NF-κB and N-cadherin protein in colon tissue of model group were up-regulated (P<0.01), while E-cadherin was significantly down-regulated (P<0.01). Compared with the model group, the changes of the above indexes in the BXD and mesalazine groups were ameliorated, with statistical differences (P<0.05 or P<0.01), and the changes in the BXD high-dose group were more significant. CONCLUSION BXD exhibits strong anti-inflammatory and anti-tumor benefits in CAC mice, inhibiting macrophage activation in colon tissue and promoting M2 polarization, while reducing the expression of tumor associated proteins PCNA and Bcl-2, and block the progression of EMT related proteins (E-cadherin and N-cadherin). The mechanism may connect to suppressing NF-κB P65 and IκB-α activation to regulate the NF-κB signaling pathway.

OBJECTIVE To investigate the effect of Banxia Xiexin decoction(BXD) on colitis associated cancer(CAC) mice and its related mechanism. METHODS Seventy-five C57BL/6 mice were randomly divided into normal group, model group, Banxia Xiexin decoction low-dose group, high-dose group and mesalazine group. Except for the normal group, the mice in the other groups were intraperitoneally injected with azoxymethane combined with oral dextran sodium sulfate to establish the CAC model. BXD and mesalazine were given respectively for intervention. The general conditions of all mice were observed and recorded, and the changes of body weight, disease activity index, colon length and tumor number were monitored. HE staining was utilized to observe the pathological changes of colon tissue. The expression levels of PCNA, NF-κB P65 and IκB-α were detected by immunohistochemistry. The mRNA levels of IL-17A, N-cadherin, E-cadherin and Bcl-2 were detected by qRT-PCR. Macrophage infiltration was measured using immunostaining analysis. Western blotting was applied to analyze the expression of NF-κB, E-cadherin and N-cadherin proteins in colon tissues of each group. RESULTS There was no significant tumor occurrence in the normal group, while the body weight of the model group mice was significantly reduced and the number of colon tumors increased. The colon length, number of tumors, and degree of inflammatory cell infiltration in the BXD group were significantly improved compared to the model group. Immunohistochemical results showed that the expression of PCNA, NF-κB P65 and IκB-α protein in colon tissue of model group was remarkably increased (P<0.01). Immunofluorescence results showed that the number of F4/80, CD80 and CD206 positive macrophages in the colon tissue of the model group increased (P<0.05 or P<0.01). The results of RT-PCR demonstrated that the levels of IL-17A, N-cadherin and Bcl-2 mRNA in the colon tissue of the model group were significantly increased (P<0.01), while the level of E-cadherin mRNA was fundamentally decreased (P<0.01). Western blotting results displayed that the expression levels of NF-κB and N-cadherin protein in colon tissue of model group were up-regulated (P<0.01), while E-cadherin was significantly down-regulated (P<0.01). Compared with the model group, the changes of the above indexes in the BXD and mesalazine groups were ameliorated, with statistical differences (P<0.05 or P<0.01), and the changes in the BXD high-dose group were more significant. CONCLUSION BXD exhibits strong anti-inflammatory and anti-tumor benefits in CAC mice, inhibiting macrophage activation in colon tissue and promoting M2 polarization, while reducing the expression of tumor associated proteins PCNA and Bcl-2, and block the progression of EMT related proteins (E-cadherin and N-cadherin). The mechanism may connect to suppressing NF-κB P65 and IκB-α activation to regulate the NF-κB signaling pathway.

Objective To investigate the protective effect of resveratrol on intestinal barrier in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced Parkinson's disease(PD)mouse models and its mechanism for regulating TLR4/MyD88/NF-κB signaling to protect dopaminergic neurons.Methods Fifty-two C57BL/6J mice were randomized into control group(n= 12),MPTP group(n=14),MPTP+resveratrol(30 mg/kg)group(n=13),and MPTP+resveratrol(90 mg/kg)group(n=13),and mouse models were established by intraperitoneal MPTP(30 mg/kg)injection for 7 days in the latter 3 groups.Behavioral tests were conducted to evaluate the effect of resveratrol on motor symptoms of the mice.Western blotting was used to detect the expression of TH,α-syn,ZO-1,Claudin-1,TLR4,MyD88,and NF-κB in the brain tissues of the mice.Immunohistochemistry,immunofluorescence,ELISA and transmission electron microscopy were used to verify the effect of resveratrol for suppressing inflammation and protecting the intestinal barrier.Results Compared with those in the normal control group,the mice in MPTP group showed significant changes in motor function,number of dopaminergic neurons,neuroinflammation,levels of LPS and LBP,and expressions of tight junction proteins in the intestinal barrier.Resveratrol treatment significantly improved motor function of the PD mice(P<0.01),increased the number of neurons and TH protein expression(P<0.05),down-regulated the expressions of GFAP,Iba-1,and TLR4,lowered fecal and plasma levels of LPS and LBP(P<0.05),restored the expression levels of ZO-1 and Claudin-1(P<0.01),and down-regulated the expressions of TLR4,MyD88,and NF-κB in the colon tissue(P<0.05).The mice with resveratrol treatment at 30 mg/kg showed normal morphology of the tight junction complex with neatly and tightly arranged intestinal villi.Conclusion Resveratrol repairs the intestinal barrier by inhibiting TLR4/MyD88/NF-κB signaling pathway-mediated inflammatory response,thereby improving motor function and neuropathy in mouse models of MPTP-induced PD.

Objective To construct a novel enzyme-free colorimetric biosensor(T-CHA)based on tri-ple-helix molecular probe(THMP)and catalytic hairpin assembly(CHA)reaction for visual detection and precise quantitative analysis of low-abundance alpha-fetoprotein(AFP).Methods The absorbance produced by AFP induced T-CHA system was recorded by gel electrophoresis and ultraviolet-visible spectrophotometer to evaluate the feasibility of T-CHA strategy.The molar concentration ratio of THMP and CHA,reaction time of CHA,temperature and pH value of buffer solution were optimized respectively.The color reaction of T-CHA was induced by different concentrations of AFP to explore the detection efficiency of T-CHA.Results Under the op-timal experimental conditions,the logarithmic values of AFP at different concentrations showed a linear rela-tionship from 5 μg/mL to 10 ng/mL,and the detection limit was 2.29 μg/mL.The T-CHA system could com-plete accurate quantitative analysis of low abundance AFP and visual free-labeled detection within 105 min,moreover the sensitivity of T-CHA was superior to that of ELISA.Conclusion Utilizing the low background leakage of THMP and the high catalytic efficiency of CHA,the T-CHA system could realize the early accurate diagnosis of hepatocellular carcinoma,moreover which has a certain application prospect in the real time detec-tion.

Objective:To evaluate the relationship between the mechanism of curcumin attenuating lidocaine-induced neurotoxicity and autophagy.Methods:In vitro human neuroblastoma SH-SY5Y cells at the logarithmic phase were divided into 3 groups ( n=12 each) using the random number table method: blank control group (C group), lidocaine group (Lid group), and curcumin + lidocaine group (Cur + Lid group). The cells were incubated with complete medium containing 1.0 μmol/L curcumin for 24 h, and the other groups were incubated with fresh medium for 24 h under the same conditions in Cur+ Lid group. Then the medium was incubated with the complete medium containing 4.0 mmol/L lidocaine for 24 h in Lid and Cur+ Lid groups, and the medium was replaced with the fresh medium and the cells were incubated for 24 h under the same conditions in group C. At the end of incubation or culture, the cell viability was detected by CCK-8 method, the level of autophagosomes was detected by the MDC method, and the expression of P62, microtubule-associated protein light chain 3-Ⅱ (LC3-Ⅱ) and LC3-Ⅰ was detected by Western blot, and the LC3-Ⅱ/LC3-Ⅰ ratio was calculated. Results:Compared with group C, the cell viability was significantly decreased, the level of autophagosomes was increased, the expression of LC3-Ⅱ was up-regulated, the expression of LC3-Ⅰ was down-regulated, the LC3-Ⅱ/LC3-Ⅰ ratio was increased, and the expression of P62 was down-regulated in Lid and Cur+ Lid groups ( P<0.05). Compared with Lid group, the cell viability and level of autophagosome were significantly increased, the expression of LC3-Ⅱ was up-regulated, the expression of LC3-Ⅰ was down-regulated, the LC3-Ⅱ/LC3-Ⅰ ratio was increased, and the expression of P62 was down-regulated in Cur+ Lid group ( P<0.05). Conclusions:The mechanism by which curcumin reduces the neurotoxicity induced by lidocaine may be related to the activation of autophagy.