Phytochemicals,Essential Oils Composition and Antioxidant Activity of Astragalus spp., Phlomis olivieri and Daphne mucronata in Habitats of Central Iran

This study evaluated several secondary metabolites, essential oils (EOs) compositions, and antioxidant activity in four medicinal plants that originated in Isfahan rangelands. The species were Astragalus verus, Astragalus adscendens, Daphne mucronata, and Phlomis olivieri. Thirty-two genotypes of these species were evaluated for different biochemical traits. Based on the evaluation of EOs compounds, GC/MS analysis revealed the total number of identified compounds. These compounds were 25, 22, 12, and 22 for A. adscendens, A. verus, D. mucronata, and P. olivieri, respectively. The dominant compounds were phthalate (59.88 %) in A. adscendens, phytol (38.02 %) in A. verus, hexanoic acid (32.05 %) in D. mucronata and β-cubebene (30.94 %) in P. olivieri. Phytochemical analysis showed that D. mucronata, A. adscendens, and P. olivieri had the highest total phenolics content (TPC) (18.24 mg gallic acid equivalent/g dry weight), total flavonoids content (5.57 mg QE/g DW), and total anthocyanins content (0.23 mg/g DW), respectively. The highest total chlorophyll (0.27 mg/g DW), total carotenoids (0.03 mg/g DW), and antioxidant activity (71.36 %) were observed in A. adscendens, A. adscendens and A. verus, respectively. Among all genotypes, the highest TPC (20.1 mg GAE/g DW) was observed in genotype 5 of D. mucronata. This study provided new information on the chemical compounds within the distribution range of these ecologically dominant rangeland species in Isfahan province, Iran. The data revealed that superior genotypes from these species are rich in natural antioxidants and bioactive compounds. Thus, they can be used in ethno pharmacological fields, food, and industrial applications.     

Activity and function in lung injuries due to sulphur mustard

Aim. Pulmonary complications are known to occur in over half the patients exposed to sulphur mustard. Many studies have focused on the clinical complications, often ignoring the pathogenesis of sulphur mustard. Also, the reasons for the variable severity of lung injuries caused by sulphur mustard are unclear. Hence, the current study was performed to evaluate the correlation between superoxide dismutase (SOD) and catalase (CAT) activity and pulmonary function in patients exposed to sulphur mustard. Methods. Our study was a comparative cross-sectional survey. Two hundred and fifty incident survivors were selected from the Sardasht population who were exposed to sulphur mustard in 1987. A control group from non-exposed civilians was also selected. We used a pulmonary function test, and SOD and CAT activity was measured in these groups. Results. The mean SOD activity in the healthy control group (70.5±10.8 U ml^?1) was higher than in the moderate-to-severe group (67.0±6.1 U ml^?1) (p <0.001, one-tail ANOVA, least significant difference (LSD) post hoc). The mean activity in the mild group (72.5±6.9 U ml^?1) was no higher than in the healthy control group (70.5±10.8 U ml^?1) (p=0.095 one-tail ANOVA, LSD post hoc). The mean CAT activity in the healthy control group (4.9±1.5 U ml^?1) was lower than in the moderate-to-severe group (8.0±1.8 U ml^?1) (p <0.001, one-tail ANOVA, LSD post hoc) and in the mild group (7.5±1.5 U ml^?1) (p=0.012 one-tail ANOVA, LSD post hoc). Conclusion. According to our findings, it is reasonable to hypothesize that re-establishment of the activation–inactivation or oxidant–antioxidant balance in favour of the activation and antioxidant balances would be useful as a therapeutic strategy to suppress pathological mechanisms underlying lung injuries.     

Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells

Background

Cigarette smoking is the major risk factor for COPD, leading to chronic airway inflammation. We hypothesized that cigarette smoke induces structural and functional changes of airway epithelial mitochondria, with important implications for lung inflammation and COPD pathogenesis.

Methods

We studied changes in mitochondrial morphology and in expression of markers for mitochondrial capacity, damage/biogenesis and fission/fusion in the human bronchial epithelial cell line BEAS-2B upon 6-months from ex-smoking COPD GOLD stage IV patients to age-matched smoking and never-smoking controls.

Results

We observed that long-term CSE exposure induces robust changes in mitochondrial structure, including fragmentation, branching and quantity of cristae. The majority of these changes were persistent upon CSE depletion. Furthermore, long-term CSE exposure significantly increased the expression of specific fission/fusion markers (Fis1, Mfn1, Mfn2, Drp1 and Opa1), oxidative phosphorylation (OXPHOS) proteins (Complex II, III and V), and oxidative stress (Mn-SOD) markers. These changes were accompanied by increased levels of the pro-inflammatory mediators IL-6, IL-8, and IL-1β. Importantly, COPD primary bronchial epithelial cells (PBECs) displayed similar changes in mitochondrial morphology as observed in long-term CSE-exposure BEAS-2B cells. Moreover, expression of specific OXPHOS proteins was higher in PBECs from COPD patients than control smokers, as was the expression of mitochondrial stress marker PINK1.

Conclusion

The observed mitochondrial changes in COPD epithelium are potentially the consequence of long-term exposure to cigarette smoke, leading to impaired mitochondrial function and may play a role in the pathogenesis of COPD.     

Co-delivery of miRNA-15a and miRNA-16–1 using cationic PEGylated niosomes downregulates Bcl-2 and induces apoptosis in prostate cancer cells

Biotechnology Letters - Tumor suppressor miRNAs, miR-15a and miR-16–1, with high-specificity and oncogenic targeting of Bcl-2, can target tumor tissues. Disadvantages of the clinical...     

Insight into morphological and molecular variations across Iranian spinach landraces

Molecular Biology Reports - Spinach is salt-tolerant leafy vegetable stemmed from central Asia. It has been well adapted to different climates of Iran. We aimed to study genetic diversity between...     

Perspectives on the use of multiple sclerosis risk genes for prediction

Objective

A recent collaborative genome-wide association study replicated a large number of susceptibility loci and identified novel loci. This increase in known multiple sclerosis (MS) risk genes raises questions about clinical applicability of genotyping. In an empirical set we assessed the predictive power of typing multiple genes. Next, in a modelling study we explored current and potential predictive performance of genetic MS risk models.

Materials and Methods

Genotype data on 6 MS risk genes in 591 MS patients and 600 controls were used to investigate the predictive value of combining risk alleles. Next, the replicated and novel MS risk loci from the recent and largest international genome-wide association study were used to construct genetic risk models simulating a population of 100,000 individuals. Finally, we assessed the required numbers, frequencies, and ORs of risk SNPs for higher discriminative accuracy in the future.

Results

Individuals with 10 to 12 risk alleles had a significantly increased risk compared to individuals with the average population risk for developing MS (OR 2.76 (95% CI 2.02–3.77)). In the simulation study we showed that the area under the receiver operating characteristic curve (AUC) for a risk score based on the 6 SNPs was 0.64. The AUC increases to 0.66 using the well replicated 24 SNPs and to 0.69 when including all replicated and novel SNPs (n = 53) in the risk model. An additional 20 SNPs with allele frequency 0.30 and ORs 1.1 would be needed to increase the AUC to a slightly higher level of 0.70, and at least 50 novel variants with allele frequency 0.30 and ORs 1.4 would be needed to obtain an AUC of 0.85.

Conclusion

Although new MS risk SNPs emerge rapidly, the discriminatory ability in a clinical setting will be limited.