Zn-coordination polymers for fluorescence sensing various contaminants in water.

Luminescent coordination polymers (LCPs) have garnered significant attention from researchers as promising materials for detecting contaminants. In this paper, three new LCPs ([Zn(tib)(opda)]n⋅H2O (1), [Zn3(tib)2(mpda)3]n⋅5H2O (2), [Zn (tib)(ppda)]n⋅H2O (3)) with different structures (LCP 1-3: 1D, 2D, 1D) using phenylenediacetic acid isomers and 1,3,5-tris (1-imidazolyl) benzene (tib) are synthesized. The specific surface areas (BET) of LCP 1-3 are 4 m2/g, 19 m2/g, and 13 m2/g respectively. LCP 1-3 exhibit excellent fluorescence properties and can serve as fluorescent probe for the detection of inorganic contaminants and organic contaminants. Due to the large BET of LCP 2, the detection limits for trace analytes surpass those of LCP 1 and 3. The detection limits of LCP 2 for Fe3+, nitrobenzene (NB), chloramphenicol (CAP), and pyrimethanil (PTH) are 8.3 nM, 0.016 µM, 0.19 µM, and 0.032 µM, respectively, and the fluorescence quenching rates are 98.6 %, 98.8 %, 92.3 %, and 98.8 %, respectively. These values outperform most reported in the literature. The quantum yields of LCP 1-3 are 11.84 %, 25.22 %, 22.00 % respectively. Real sample testing of LCP 1-3 reveals favorable performance, where spiked recoveries of LCP 2 for the detection of pyrimethanil in grape skins ranged from 99.62 % to 119.3 % with a relative standard deviation (RSD) of 0.627 % to 4.56 % (n = 3). The fluorescence quenching mechanism was attributed to a combination of photoelectron transfer (PET), resonance energy transfer (RET), and competitive absorption (CA). This study advances the application of LCPs in luminescence sensing and contributes to the expansion of novel materials for detecting environmental pollutants.

Effects of traditional artiri La Li formulation on experimental models of vitiligo and mechanisms of melanogenesis.

ETHNOPHARMACOLOGICAL RELEVANCE: Artiri La Li Honey Pill (ALLHP) is a traditional medicinal formula that is widely used in Xinjiang, China, for the treatment of vitiligo. Since the cause of vitiligo has not been determined, no satisfactory treatment is available. Clinical interventions include pharmacological treatment with psoralen, usually in conjunction with ultraviolet A (UVA) radiation, but toxic side effects limit this application. Studies on the activity and mechanisms of ALLHP are scarce. AIM OF THE STUDY: To verify the therapeutic effect of ALLHP on vitiligo and determine its effectiveness as a theoretical and experimental basis for the development of innovative drugs with independent intellectual property rights and the effective use of local resources. MATERIALS AND METHODS: The experimental animal model of vitiligo was established by chemical decoloring. Rats were treated with gradient doses of ALLHP. The therapeutic effect was judged by gross observation. The contents of TYR, MAO, AchE and MDA in serum and skin tissue, the number of hair follicles containing melanin in skin tissue, the distribution of epidermal melanin, and the weight index of immune organs were detected, and the therapeutic effect of ALLHP on vitiligo was evaluated. In addition, certain monomer components in ALLHP were used to intervene in the zebrafish juvenile melanin suppression model, and the melanin-activating activities of some monomer components in ALLHP were screened by counting the melanin area ratio. RESULTS: ALLHP increased the number of melanin-containing hair follicles and the epidermal melanin content in the skin of experimental vitiligo animals, repaired the skin cell morphology to a certain extent, increased the content of TYR in serum and skin, and reduced the content of MDA, AchE and MAO. Carvone, Luteolin, Psoralen and Psoraleae phenol and Bakuchiol could increase the melanin area of experimental melanin inhibition in zebrafish. CONCLUSION: According to the results of this study, ALLHP can increase the number of melanin-containing hair follicles and the epidermal melanin content in the skin of vitiligo animals and restore skin cell morphology to a certain extent by reducing oxidative stress in epidermal tissue. A wide range of active ingredients may promote melanogenesis with ALLHP.

Potential anti-vitiligo properties of cynarine extracted from Vernonia anthelmintica (L.) Willd.

Vitiligo is a depigmentation disorder of the skin. It is primarily caused by the destruction of melanocytes or obstruction of the melanin synthesis pathway. Melanin is a type of skin pigment that determines skin color. The seeds of Vernonia anthelmintica (L.) Willd (Kaliziri) are used for treating skin diseases including vitiligo in traditional Uyghur medicine. 1,5­Dicaffeoylquinic acid (1,5­diCQA) is a natural polyphenolic compound widely distributed in plants and extracted from Kaliziri seeds. Therefore, in the present study, the effect of 1,5­diCQA on melanin synthesis in B16 cell was evaluated, and its molecular mechanism was explored. The results indicated that 1,5­diCQA treatment of B16 cells stimulated an increase of intracellular melanin level and tyrosinase (TYR) activity without cytotoxicity. Reverse transcription quantitative polymerase chain reaction results also indicated that 1,5­diCQA may markedly improve the protein expression and RNA transcription of microphthalmia­associated transcription factor (MITF), melanogenic enzyme Tyr, tyrosinase­related protein 1 (TRP 1) and tyrosinase­related protein 2 (TRP 2). Additional results identified that 1,5­diCQA may promote the phosphorylation of p38 mitogen­activated protein kinase (p38 MAPK) and extracellular signal­regulated kinase (ERK) MAPK. Notably, the increased levels of intracellular melanin synthesis and tyrosinase expression induced by 1,5­diCQA treatment were significantly attenuated by the protein kinase A (PKA) inhibitor H­89. Intracellular cyclic adenosine monophosphate (cAMP) concentration and phosphorylation of cAMP­response element binding protein was increased following 1,5­diCQA treatment. These results indicated that 1,5­diCQA stimulated melanogenesis via the MAPK and cAMP/PKA signaling pathways in B16 cells, which has potential therapeutic implications for vitiligo.

[Effect of Autophagy on Homoharringtonine-treated K562 Cells].

OBJECTIVE: To study the effect of homoharringtonine (HHT) alone or combined with 3-methyladenine (3-MA) , an autophagy inhibitor, on the apoptosis and autophagy of K562 cells. METHODS: K562 cells were treated with HHT(10 ng/ml) or HHT(10 ng/ml) combined with 3-MA (1.5 mmol/L) for 1 to 8 days. The apoptosis of treated cells was tested by means of flow cytometry(FCM), and the autophagy levels were tested with RT-PCR, Western blot and electron microscopy. RESULTS: In the early stage of HHT-treated group, the apoptosis rate increased and decreased later. Beclin1 mRNA expression level and the LC3II/I ratio were declined firstly and increased later in HHT group. While combining with autophagy inhibitor 3-MA, both the Beclin1 mRNA expression level and the LC3II/I ratio were declined continually during the treated period. The activated caspase-3 protein expression level was also raised sustainability during both HHT and 3-MA cultured period. CONCLUSIONS: HHT can induce apoptosis of K562 cells, but the sustaining effect of HHT can induc autophagy of K562 cells, the combination of HHT with 3-MA may enhance the cytotoxicitic effect of HHT on K562 cells.

[Effect of Homoharringtonine Combined with Imatinib on the K562/G01 Cells and Its Mechanism].

OBJECTIVE: To explore the effect of homoharringtonine(HHT) combined with imatinib(IM) on proliferation and apoptosis of K562/G01 cells and its potential mechanism. METHODS: K562/G01 cells were cultured with HHT and/or IM. CCK-8 assay was used to detect cell proliferation. Cell apoptosis and phosphorylated tyrosine levels were analyzed by flow cytometry. The expression levels of p210, PI3K, p-Akt and Akt protein were determined by Western blot. RESULTS: Compared with HHT or IM alone, drug combination significantly inhibited cell proliferation and induced apoptosis of K562/G01 cells (both P< 0.05). HHT combined with IM could inhibit the levels of phosphorylated tyrosine and phosphorylated Crkl and downregulate the expressions of p210, PI3K and p-Akt in K562/G01 cells. CONCLUSION: HHT combined with IM can synergistically inhibit proliferation and induce apoptosis of K562/G01 cells by suppressing the p210 expression and its kinase activity.

[Time rhythm of homoharringtonine inducing K562 cell apoptosis and its mechanism].

This study was aimed to explore the change of K562 cell apoptosis at different time point after homoharringtonine (HHT) treatment and its mechanism. After treatment of K562 cells with 10 ng/ml HHT, the cell viability was tested with MTT assay; the expression of caspase-3 was detected with Western blot; the BCL-2 expression was analyzed with flow cytometry; the autophagosome was observed by electron microscopy. The results showed that the viability of K562 cells reduced gradually from day 1 to day 5 and ascended from day 6 to day 8 after HHT treatment. At the same time, the cleaved caspase-3 expression level of K562 cells increased gradually from day 1 to day 7, but reduced at the day 8 (P < 0.05). From day 1 to day 8 after HHT treatment, the BCL-2 expression level declined firstly and then went up (P < 0.05). Autophagosome was also seen remarkably at day 8 after HHT treatment. It is concluded that the apoptosis level of K562 cells after being treated with HHT enhances firstly and then declines , which may be associated with higher autophagy level in the late stage of HHT treatment.

[Inhibitory effects of luteolin on human gastric carcinoma xenografts in nude mice and its mechanism].

OBJECTIVE: To explore the in vivo anticancer effects of luteolin with BGC-823 gastric carcinoma xenografts in nude mice and elucidate its mechanism. METHODS: After modeling of gastric carcinoma xenografts in nude mice, 40 BALB/c (nu/nu) nude mice were randomly divided into 5 groups (n = 8 each). And an intraperitoneal injection of luteolin was administered at 10 mg/kg (low-dose), 20 mg/kg (middle-dose) and 40 mg/kg (high-dose) groups. And 5-fluorouracil (30 mg/kg) and control groups were also established. The growth curves of xenografts in nude mice were drawn and weight inhibition rates measured. The morphological features were detected by hematoxylin and eosin staining. And the protein expression levels of vascular endothelial growth factor A (VEGF-A) and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry. RESULTS: In vivo tumor formation test showed that tumor volume in nude mice treated with luteolin was smaller than that of control group. Tumor weights of high-dose luteolin group were lighter than those of the control ((0.29 ± 0.01) vs (0.38 ± 0.03) g). And the difference was statistically significant (P < 0.01). The rate of tumor inhibition in high-dose luteolin group was up to 24.87%. Lymphocytic invasion of tumor tissue was observed under light microscope in the treatment groups. Results of immunohistochemistry showed the positive cell integral of VEGF in middle and high-dose luteolin groups were 1.25 ± 0.17 and 1.00 ± 0.07 respectively. Both were significantly lower than that of control group (1.50 ± 0.15, both P < 0.05). The positive cell integral of MMP-9 in high-dose luteolin group was markedly lower than that of control group (3.75 ± 1.43 vs 9.00 ± 1.08, P < 0.01). CONCLUSIONS: Luteolin can effectively inhibit the in vivo growth of gastric tumor. The mechanism may be correlated with the stimulation of immune response and the down-regulated expressions of VEGF-A and MMP-9.

[Plasma gamma-glutamyl transpeptidase level as a cardiovascular risk factor in elderly patients with hypertension or hypertension with diabetes mellitus].

OBJECTIVE: To investigate plasma gamma-glutamyl transpeptidase (γ-GGT) level as a cardiovascular risk factor in elderly patients with hypertension or hypertension with diabetes mellitus. METHODS: Forty-nine elderly patients of hypertension and 42 elderly patients of hypertension with diabetes mellitus and 39 healthy elderly subjects were enrolled in the study. The height, weight and blood pressure of patients were measured, serum C reactive protein and other biochemical indicators were detected. The relation between plasma γ-GGT and cardiovascular risk factors in three groups were analyzed. RESULTS: There was no significant difference in plasma γ-GGT levels among three groups. There was a positive correlation of plasma γ-GGT levels with systolic pressure, pulse pressure, hemoglobin A1c and CRP in control group. While in hypertension with diabetes mellitus group, plasma γ-GGT levels were correlated with systolic pressure, mean arterial pressure, fasting blood sugar and cystatin. CONCLUSION: Plasma γ-GGT might be a risk factor for cardiovascular diseases, and may be used as a predictive indicator for kidney injury in early patients with hypertension with diabetes mellitus.

[Changes of blood pressure, blood glucose and blood lipids levels after intensive treatment in incipient diabetes II patients].

OBJECTIVE: To evaluate the effect of intensive treatment on the blood sugar, blood lipids and blood pressure levels in incipient diabetes II patients. METHODS: One hundred and sixty incipient diabetes patients were allocated into two groups according to chronological order: 80 cases received routine treatment and 80 cases received intensive treatment. Fasting blood-glucose (FBG), glycosylated hemoglobin (HbA1C), blood pressure, blood cholesterol (TC), triglyceride (TG), LDL cholesterol-C (LDL-C), alanine aminotransferase (ALT) and aspertate aminotransferase (AST) were tested before treatment. For intensive treatment group blood pressure, blood sugar and blood lipids were regularly tested, and the therapeutic protocols were adjusted according to the test results until the therapeutic target reached. After six months, HbA1C, blood pressure, TC, LDL-C, ALT and AST were tested again and comparison was made between the two groups. RESULTS: There was a significant decrease in TC and LDL-C in the intensive treatment group compared with those in the routine treatment group (P <0.05). CONCLUSION: The intensive treatment on the incipient diabetes II patients facilitate the control of the blood lipids and blood sugar.

[Effect of thymosin alpha 1 on cellular immune function in elderly patients with malignant tumor].

OBJECTIVE: To investigate the effect of thymosin alpha 1 on cellular immune function in the elderly patients with malignant tumor. METHODS: Thirty patients with malignant tumor were injected with thymosin alpha 1 subcutaneously at the dose of 1.6 mg q.d. for the first month and q.o.d. for the following month. The number of T cell subgroups and the activity of NK cell in peripheral blood were detected and the quality of life of the patients were evaluated before treatment and at the end of treatment. RESULT: Treatment of thymosin alpha 1 increased the number of CD4 cells and improved the NK activity, and also improved the quality of life of the elderly patients with malignant tumor. There were no side effects found. CONCLUSION: Thymosin alpha 1 can enhance the cellular immune function of the elderly patients with malignant tumor.

[Inhibition of intracellular Ca(2+)-chelating agent on Hela cell apoptosis induced by HSV-1].

AIM: To explore the variation of intracellular free-Ca (2+) concentration during Hela cell apoptosis induced by HSV-1 and inhibition of Ca(2+)-chelating agent on the apoptosis. METHODS: Apoptosis of the Hela cells infected by HSV-1 was observed under scanning electron microscope (SEM) and transmission electron microscope (TEM), and the variation of intracellular free-Ca (2+) concentration, labeled with fluorescent probe was observed under fluorescence-microscope at a series of timepoints. RESULTS: The Hela cells infected by HSV-1 showed typical apoptotic morphological changes. Free-Ca (2+) concentration increased and reached peak at the 12 hours after HSV-1 infection. Characteristic morphological features of apoptosis occurred at the 24 hours after infection. This apoptosis could be inhibited by intracellular Ca(2+)-chelating agent. CONCLUSION: Intracellular free-Ca(2+) might play an important role in Hela cell apoptosis induced by HSV-1, which provides useful clues for clinical treatment of associated diseases.