Combined Antioxidant, Anti-inflammaging and Mesenchymal Stem Cell Treatment: A Possible Therapeutic Direction in Elderly Patients with Chronic Obstructive Pulmonary Disease.

Chronic Obstructive Pulmonary Disease (COPD) is a worldwide health problem associated with high morbidity and mortality, especially in elderly patients. Aging functions include mitochondrial dysfunction, cell-to-cell information exchange, protein homeostasis and extracellular matrix dysregulation, which are closely related to chronic inflammatory response and oxidation-antioxidant imbalance in the pathogenesis of COPD. COPD displays distinct inflammaging features, including increased cellular senescence and oxidative stress, stem cell exhaustion, alterations in the extracellular matrix, reduced levels of endogenous anti-inflammaging molecules, and reduced autophagy. Given that COPD and inflammaging share similar general features, it is very important to identify the specific mechanisms of inflammaging, which involve oxidative stress, inflammation and lung mesenchymal stem cell function in the development of COPD, especially in elderly COPD patients. In this review, we highlight the studies relevant to COPD progression, and focus on mechanisms associated with inflammaging.

Pyrroloquinoline quinone delays inflammaging induced by TNF-α through the p16/p21 and Jagged1 signalling pathways.

Previous studies on the longevity effect of pyrroloquinoline quinine (PQQ) on nematode worms have revealed that PQQ can enhance the antioxidant capacity of nematode worms, thus extending the lifespan of the worms. The induction and development of cellular senescence are closely connected with inflammatory reactions. The aim of this study was to determine the effect of PQQ and ageing factors on senescent cells. To this end, we cultivated human embryonic lung fibroblasts in nutrient solution with or without tumour necrosis factor-alpha (TNF-α) to establish an inflammaging model in vitro. The cells were preincubated with or without PQQ to determine if PQQ had any anti-inflammaging effect. More senescent cells were detected with the addition of TNF-α than without (P < .01). The ratio of senescent cells to non-senescent cells in the TNF-α group was greater than that in the control group (P < .01). When cells were preincubated with PQQ prior to TNF-α treatment, there were fewer senescent cells than those in the control group, which was not pretreated with PQQ (P < .05). The same tendency was noted with regard to p21, p16, and Jagged1. In summary, we used TNF-α, a well-known pro-inflammatory cytokine associated with inflammaging, to establish an in vitro inflammaging model and provided evidence that PQQ delays TNF-α -induced cellular senescence and has anti-inflammaging properties.

Characteristics of Long Noncoding RNAs in the Pancreas of Rats With Acute Pancreatitis.

OBJECTIVE: Long noncoding RNAs (lncRNAs) have received increasing attention as potential regulators of several biological processes. However, the precise effects of lncRNAs in acute pancreatitis (AP) have seldom been studied. This study aimed to describe the microarray-based differential expression profile of messenger RNA (mRNAs) and lncRNAs in AP and identify candidate biomarkers for the diagnosis, prognosis, and treatment of AP. METHODS: A rat model of AP was generated with retrograde pancreatic ductal injection of sodium taurocholate, and the pancreas was harvested for microarray detection. The biological functions of differentially expressed mRNAs noted from microarray data were assessed by bioinformatics analysis. A coding-noncoding gene coexpression network was built for the most promising mRNAs, from which 10 lncRNAs were selected for subsequent validation by real-time quantitative reverse transcription polymerase chain reaction. RESULTS: There were 1156 lncRNAs and 3022 mRNAs distinctively dysregulated in rats with AP relative to the controls. The significantly enriched Gene Ontology term associated with upregulated mRNAs was immune system process. Kyoto Encyclopedia of Genes and Genomes functional analysis demonstrated that the upregulated transcripts were highly enriched in natural killer cell-mediated cytotoxicity. CONCLUSIONS: Further research is needed to establish lncRNAs uc.308-, BC158811, BC166549, BC166474, and BC161988 as diagnostic and therapeutic targets.