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Camellia nitidissima Chi (CNC), belonging to Camellia genus (Theaceae family), is a medicinal and edible plant in China. Among the whole plant, the CNC flowers are especially precious, but the biological activities and the compositions of the CNC flowers are unknown. In this study, inhibiting effects on the formation of advanced glycation end-products (AGEs) of five CNC flowers fractions and three isolated compounds were investigated, these three compounds are two flavonoid glycosides and one flavanol, namely kaempferol 3-O-[2,3,4-Tri-O-acetyl-α-L-rhamnopyranosyl-(1→3)-2,4-di-O-acetyl-α-L-rhamnopyranosyl-(1→6)]-β-D-glucopyranoside, kaempferol 3-O-[2,3,4-Tri-O-acetyl-α-L-rhamnopyranosyl-(1→3)-4-O-acetyl-α-L-rhamnopyranosyl-(1→6)]-β-D-glucopyranoside and catechin. Among these five fractions, the ethyl acetate fraction showed the highest total phenolic contents and inhibiting effects on AGE formation. Bovine serum albumin (BSA)-glucose and BSA-methylglyoxal assay showed that the ethyl acetate fraction inhibited AGE formation by 74.49% and 34.3% at 1 mg/mL, respectively. As the main components, these three compounds also showed remarkable inhibiting effects on AGE formation by scavenging methylglyoxal, next two catechin-carbonyl adducts were identified using HPLC-ESI-MS/MS. The results showed that the CNC flowers had remarkable inhibiting effects on the formation of AGEs. The primary structure-activity relationship showed (1) the glycosides could reduce the inhibiting effects compared to kaempferol and (2) the acetyl at position 2‴ in compound 1 had no remarkable influence of the inhibiting effects on AGE formation compared to compound 2. [Display omitted] •C. nitidissima Chi (CNC) is one medicinal and edible plant in China.•CNC flowers had effects on inhibiting AGE formation by scavenging methylglyoxal.•Two flavonoid glycosides and one flavanol had effects on inhibiting AGE formation.•Two catechin-carbonyl adducts were identified by HPLC-ESI-MS/MS.

In vitro toxicology research into the health effects of atmospheric particulate matter (PM) depends on the extraction of PM from filters. Previously, we proposed an efficient PM sampling and extraction method based on low-cost agar membrane and performed an exposure study with RAW264.7 macrophages. Here, we extended the application of this strategy, employing lung and hepatic cells, to validate its reliability and reproducibility. One traditional strategy using polytetrafluoroethylene (PTFE) filter was adopted for comparison. Cytotoxicity and proteomics results showed that the PM extracted by two methods induced comparable toxicity to A549 and BEAS-2B cells, while the PM extracted from the agar membranes induced higher toxicity to HepG2 and HL7702 cells than that from the PTFE filters. The differences in the investigations might be associated with the cell's sensitivity to the extracted suspended particles. This work indicated the importance of assessing PM cytotoxicity from the perspective of extraction methods and cell lines.

Zinc oxide nanoparticle is one of the nanomaterials people engaged most in their life and its health effect has been taken into concern. In this work, A549 cell line was used as cell model, and the cytotoxicity of zinc oxide nanoparticles was revealed to be concentration-dependent. Through the measurement of cellular proteome, much more differentially expressed proteins were observed after the cells being treated for 9 h than 24 h. Also, most of these proteins expressed in the pattern which showed a significant decrease after exposure to zinc oxide nanoparticles and then an increase at 24 h. Intracellular reactive oxygen species and glutathione determination indicated that high level of oxidative stress was presented in cell after treatment with zinc oxide nanoparticles for 9 h. It can be observed from western blot analysis that the expression of NF-κB p65, PNPase, and HSP90 rose significantly after 9 h of exposure. Thus, a deduction was reached that toxicity of nanoparticles consists both of particle toxicity and ion toxicity, and a long-time treatment may conceal the toxicity induced by particles. The conclusion we made highlighted the importance of exposure time in the study of nanoparticle toxicity and would provide a new perspective for studying toxicity mechanism of nanoparticles.

Objective： To assess the effect of angiotensin II type 1 （AT1） receptor antagonist losartan on myocardium connexin43 （Cx43） gap junction （GJ） expression in spontaneously hypertensive rats （SHRs） and investigate possible mechanisms. Methods： Sixteen 9-week-old male SHRs and 8 age-matched male Wistar-Kyoto （WKY） rats were included in this study. SHRs were randomly divided into two groups to receive losartan at 30 mg/（kg·d） by oral gavage once daily for 8 weeks （SHR-L） or vehicle （0.9% saline） to act as controls （SHR-V）; WKY rats receiving vehicle for 8 weeks served as normotensive controls. At the end of the experiment, rats were sacrificed and the hearts were removed. Expressions of Cx43 and nuclear factor-kappaB p65 （NF-κB p65） proteins in all three groups were observed and further investigations on the effect of angiotensin II type 1 receptor antagonist losartan （30 mg/（kg·d）, 8 weeks） on Cx43 expression were conducted with Western blot and immunohistochemistry. NF-κB p65 protein in nuclear extracts was determined by Western blot. Results： Left ventricular （LV） hypertrophy was prominent in SHRs, Cx43 and NF-κB p65 protein expressions were obviously upregulated and Cx43 distribution was dispersed over the cell surface. Treatment with losarton reduced the over-expressions of Cx43 and NF-κB p65 in LV myocardium. The distribution of Cx43 gap junction also became much regular and confined to intercalated disk after losartan treatment. Conclusion： Cx43 level was upregulated in LV myocardium of SHR during early stage of hypertrophy. Angiotensin II type 1 receptor antagonist losartan prevented Cx43 gap junction remodeling in hypertrophied left ventricles, possibly through the NF-κB pathway.

In this paper, using a piezoelectric trilaminar optimized low frequency sensing element, the authors designed a high sensitivity internal placed ICP piezoelectric accelerometer as a sensing element. Through structure optimization, they made a high sensitivity, broadband, small scale vector sensor. The working band is 10-2,000 Hz; the sound pressure sensitivity is -185 dB (at 100 Hz); the outer diameter is 42 mm; and the length is 80 mm.

Idiopathic pulmonary arterial hypertension （IPAH） is a rare disease of unknown etiology. The exact pathogenesis of pulmonary arterial hypertension is still not well known. In the past decades, many protein molecules have been found to be involved in the development of IPAH. With proteomic techniques, profiling of human plasma proteome becomes more feasible in searching for disease-related markers. In present study, we showed the protein expression profiles of the serum of IPAH and healthy controls after depleting a few high-abundant proteins in serum. Thirteen spots had changed significantly in IPAH compared with healthy controls and were identified by LC-MS/MS. Alpha- 1-antitrypsin and vitronectin were down-regulated in IPAH and may be valuable candidates for further explorations of their roles in the development of IPAH.

Idiopathic pulmonary arterial hypertension (IPAH) is a rare disease of unknown etiology. The exact pathogenesis of pulmonary arterial hypertension is still not well known. In the past decades, many protein molecules have been found to be involved in the development of IPAH. With proteomic techniques, profiling of human plasma proteome becomes more feasible in searching for disease-related markers. In present study, we showed the protein expression profiles of the serum of IPAH and healthy controls after depleting a few high-abundant proteins in serum. Thirteen spots had changed significantly in IPAH compared with healthy controls and were identified by LC-MS/MS. Alpha-1-antitrypsin and vitronectin were down-regulated in IPAH and may be valuable candidates for further explorations of their roles in the development of IPAH.

Chrysanthemum indicum Linnén (C. indicum), a medicinal and food herb with various bioactive components, may be of beneficial use in cosmetics and the treatment of skin-related diseases. However, to date, few studies have been reported on its potential preventive and therapeutic effects on skin cancer. Therefore, the present study aimed to investigate the effect and potential mechanism of action of supercritical carbon dioxide extract from C. indicum (CISCFE) on UV-induced skin cancer in a mouse model. Kunming mice were allocated randomly to five treatment groups: Sham, model, low concentration CISCFE, high concentration CISCFE and positive control nicotinamide groups. The dorsal skin of mice was irradiated with UV light for 31 weeks. Histopathological changes, ELISA assays, immunohistochemical analysis and western blotting were performed to investigate the potential therapeutic effects of CISCFE. The results showed that CISCFE alleviated skin oxidative and inflammatory damage in a UV-induced mouse model of skin cancer. Moreover, CISCFE suppressed abnormal activation of proto-oncogene c-Myc and the overexpression of Ki-67 and VEGF, and increased expression of the anti-oncogene PTEN, thereby reducing abnormal proliferation of the epidermis and blood vessels. Additionally, CISCFE increased the protein expression levels of NAD-dependent protein deacetylase sirtuin-1 (SIRT1), Kelch-like ECH associated protein 1 (Keap1) and inhibited the expression of nuclear factor 2 erythroid 2-related factor 2 (Nrf2), phosphorylated (p)-p62 (Ser 349), p-p65 and acetyl-p65 proteins in a UV-induced skin cancer mouse model. In summary, CISCFE exhibited potent anti-skin cancer activity, which may be attributed its potential effects on the p62/Keap1-Nrf2 and SIRT1/NF-κB pathways.

Background Chemotherapy toxicity is a serious problem from which non‐small cell lung cancer (NSCLC) patients suffer. The mismatch repair (MMR) system is associated with platinum‐based chemotherapy toxicity in NSCLC patients. In this study, we aimed to investigate the relationship between genetic polymorphisms in the MMR pathway and platinum‐based chemotherapy toxicity in NSCLC patients. Methods A total of 220 Chinese lung cancer patients who received at least two cycles of platinum‐based chemotherapy were recruited for this study. Toxicity was evaluated in each patient after two cycles of chemotherapy. A total of 44 single nucleotide polymorphisms were selected to investigate their associations with platinum‐based chemotherapy toxicity. Results MutS homolog 2 (MSH2) rs6544991 [odds ratio (OR) 2.98, 95% confidence interval (CI) 1.20–7.40, P = 0.019] was associated with gastrointestinal toxicity in the dominant model; MSH3 rs6151627 (OR 2.38, 95% CI 1.23–4.60, P = 0.010), rs6151670 (OR 2.05, 95% CI 1.07–3.93, P = 0.031), and rs7709909 (OR 2.38, 95% CI 1.23–4.64, P = 0.010) were associated with hematologic toxicity in the dominant model. Additionally, MSH5 rs805304 was significantly associated with overall toxicity (OR 2.21, 95% CI 1.19–4.09, P = 0.012), and MSH5 rs707939 was significantly associated with both overall toxicity (OR 0.42, 95% CI 0.23–0.76, P = 0.004) and gastrointestinal toxicity (OR 0.44, 95% CI 0.20–0.96, P = 0.038) in the dominant model. Conclusion Genetic polymorphisms in the MMR pathway are potential clinical markers for predicting chemotherapy toxicity in NSCLC patients.

Aim： To investigate the possible effects of telmisartan and Iosartan on cardiac function in adriamycin （ADR）-induced heart failure in rats, and to explore the changes in plasma level of angiotensin-（1-7）[Ang-（1-7）] and myocardial expression of angiotensin II type 1/2 receptors （AT1R / AT2R） and Mas receptor caused by the two drugs. Methods： Male Sprague-Dawley rats were randomly divided into 4 groups： the control group, ADR-treated heart failure group （ADR-HF） telmisartan plus ADR-treated group （TeI＋ADR） and Iosartan plus ADR-treated group （Los＋ADR）. ADR was administrated （2.5 mg/kg, ip 6 times in 2 weeks）. The rats in the TeI＋ADR and Los＋ADR groups were treated orally with telmisartan （10 mg/kg daily po） and Iosartan （30 mg/kg daily）, respectively, for 6 weeks. The plasma level of Ang-（1-7） was determined using ELISA. The mRNA and protein expression of myocardial Mas receptor, AT1R and AT2R were measured using RT-PCR and Western blotting, respectively. Results： ADR significantly reduced the plasma level of Ang-（1-7） and the expression of myocardial Mas receptor and myocardial AT2R, while significantly increased the expression of myocardial AT2R. Treatment with telmisartan and Iosartan effectively increased the plasma level of An8-（1-7） and suppressed myocardial ATIR expression, but did not influence the expression of Mas receptor and AT2R Conclusion： The protective effects of telmisartan and Iosartan in ADR-induced heart failure may be partially due to regulation of circulating Ang-（1-7） and myocardial ATCR expression.