Objective: To investigate the trends in incidence and mortality of lung cancer in Kaihua County, Zhejiang Province from 2011 to 2022, so as to provide insights into improving lung cancer prevention and control strategy. Methods: The incidence and mortality of lung cancer in Kaihua County from 2011 to 2022 were collected through Zhejiang Provincial Chronic Disease Surveillance Information Management System. The crude incidence, standardized incidence, crude mortality and standardized mortality of lung cancer were analyzed, and the trends in incidence and mortality of lung cancer were evaluated using average annual percent change (AAPC). Results: The crude and standardized incidence of lung cancer appeared a tendency towards an increase (AAPC=5.409% and 2.957%, both P<0.05) from 2011 to 2022, with an average annual crude incidence of 75.17/105 and average annual standardized incidence of 44.37/105. Average annual crude incidence (100.16/105 vs. 48.55/105) and standardized incidence (58.03/105 vs. 30.61/105) of lung cancer was higher in males than in females (both P<0.05). The crude incidence of lung cancer in males appeared a tendency towards an increase (AAPC=2.878%, P<0.05), with no significant changing patterns seen in standardized incidence (P>0.05). The crude and standardized incidence of lung cancer in females showed a tendency towards an increase (AAPC=11.596% and 10.464%, both P<0.05). The crude incidence of lung cancer increased rapidly among residents at ages of 45 years and older, and peaked among residents at ages of 80 to 84 years (32.11/105). The crude and standardized mortality of lung cancer appeared a tendency towards a rise and decline (AAPC=1.554% and -2.491%, both P<0.05) from 2011 to 2022, with an average annual crude and standardized mortality of 52.83/105 and 29.09/105. Average annual crude mortality (77.92/105 vs. 26.10/105) and standardized mortality (43.66/105 vs. 14.33/105) of lung cancer was higher in males than in females (both P<0.05). The crude mortality of lung cancer in males appeared a tendency towards a rise, while the standardized mortality appeared a tendency towards a decline (AAPC=1.436% and -2.553%, both P<0.05). No significant changing patterns were seen in crude and standardized mortality of lung cancer in females (both P>0.05). The crude mortality of lung cancer increased rapidly among residents at ages of 50 years and older, and peaked among residents at ages of 80 to 84 years (37.26/105). Conclusions The incidence and mortality of lung cancer appeared a tendency towards an increase in Kaihua County from 2011 to 2022, and a rapid increase was seen in the incidence of lung cancer in females.

This study has investigated the effect of a potent bioflavonoid, troxerutin,on diabetes-induced changes in pro-inflammatory mediators and expression ofmicroRNA-146a and nuclear factor-kappa-B (NF-κB) signaling pathway in aortic tissueof type-I diabetic rats. Male Wistar rats were randomly divided into four groups(n = 6/each): healthy, healthy-troxerutin, diabetic, and diabetic-troxerutin. Diabeteswas induced by streptozotocin injection (60 mg/kg; intraperitoneally) and lasted 10weeks. Troxerutin (150 mg/kg/day) was administered orally for last month of experiment.Inflammatory cytokines IL-1, IL-6, and TNF-, as well as intercellular adhesionmolecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM), cyclooxygenase-II(COX-II), and inducible-nitric oxide synthase (iNOS) were measured on aortic samplesby enzyme-linked immunosorbent assay. Gene expressions for transcription factorNF-κB, interleukin-1 receptor-associated kinase-1 (IRAK-1), TNF receptor-associatedfactor-6 (TRAF-6), and microRNA-146a were determined using real-time polymerasechain reaction. Ten-week diabetes significantly increased mRNA levels of IRAK-1,TRAF-6, NF-κB, and protein levels of cytokines IL-1, IL-6, TNF-, adhesion moleculesICAM-1, VCAM, and iNOS, COX-II, and decreased expression of microRNA-146a ascompared with healthy rats (p < 0.05 to p < 0.01). However, one month treatmentof diabetic rats with troxerutin restored glucose and insulin levels, significantly decreasedexpression of inflammatory genes and pro-inflammatory mediators andincreased microRNA level in comparison to diabetic group (p < 0.05 to p < 0.01). Inhealthy rats, troxerutin had significant reducing effect only on NF-κB, TNF- and COXIIlevels (p < 0.05). Beside slight improvement of hyperglycemia, troxerutin preventedthe activation of NF-κB-dependent inflammatory signaling in

This study has investigated the effect of a potent bioflavonoid, troxerutin,on diabetes-induced changes in pro-inflammatory mediators and expression ofmicroRNA-146a and nuclear factor-kappa-B (NF-κB) signaling pathway in aortic tissueof type-I diabetic rats. Male Wistar rats were randomly divided into four groups(n = 6/each): healthy, healthy-troxerutin, diabetic, and diabetic-troxerutin. Diabeteswas induced by streptozotocin injection (60 mg/kg; intraperitoneally) and lasted 10weeks. Troxerutin (150 mg/kg/day) was administered orally for last month of experiment.Inflammatory cytokines IL-1, IL-6, and TNF-, as well as intercellular adhesionmolecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM), cyclooxygenase-II(COX-II), and inducible-nitric oxide synthase (iNOS) were measured on aortic samplesby enzyme-linked immunosorbent assay. Gene expressions for transcription factorNF-κB, interleukin-1 receptor-associated kinase-1 (IRAK-1), TNF receptor-associatedfactor-6 (TRAF-6), and microRNA-146a were determined using real-time polymerasechain reaction. Ten-week diabetes significantly increased mRNA levels of IRAK-1,TRAF-6, NF-κB, and protein levels of cytokines IL-1, IL-6, TNF-, adhesion moleculesICAM-1, VCAM, and iNOS, COX-II, and decreased expression of microRNA-146a ascompared with healthy rats (p < 0.05 to p < 0.01). However, one month treatmentof diabetic rats with troxerutin restored glucose and insulin levels, significantly decreasedexpression of inflammatory genes and pro-inflammatory mediators andincreased microRNA level in comparison to diabetic group (p < 0.05 to p < 0.01). Inhealthy rats, troxerutin had significant reducing effect only on NF-κB, TNF- and COXIIlevels (p < 0.05). Beside slight improvement of hyperglycemia, troxerutin preventedthe activation of NF-κB-dependent inflammatory signaling in

Objective To investigate the effects and mechanisms of oridonin(ORI)on human keloid-derived fi-broblasts(HKF).Methods The effects of ORI on the proliferation activity of HKF were assessed using the CCK-8 assay.The experiment was divided into control and experimental groups.Cell scratch and Transwell assays were conducted to evaluate the migration and invasion capabilities of HKF.Real-time quantitative PCR(RT-qPCR)and Western blot were used to examine the impact of ORI on the expression of extracellular matrix-related mRNA and fi-bronectin 1(FN1),α-smooth muscle actin(α-SMA),type Ⅰ collagen(COL Ⅰ),and COL Ⅲ in HKF.The ex-periment was also divided into control,model,and transforming growth factor(TGF)-β1+ORI groups.RT-qPCR and Western blot were utilized to determine the effects of ORI on the expression of TGF-β1-induced mRNA and nu-cleotide-binding oligomerization domain-like receptor protein 3(NLRP3),apoptosis-associated speck-like protein containing a CARD(ASC),Smad2,Smad3,phosphorylated Smad2(p-Smad2),and p-Smad3 in HKF.Results CCK-8 assay demonstrated that the cell inhibition rate of HKF progressively increased with increasing concentra-tions of ORI.Compared with the control group,the experimental group exhibited a significant reduction in the mi-gration area at 24 hours and a decrease in the number of invasive cells.Furthermore,there was a significant down-regulation in the expression levels of FN1,α-SMA,COL Ⅰ,and COL Ⅲ(P＜0.05).In comparison with the con-trol group,the model group showed a significant upregulation in the expression of NLRP3,ASC,Smad2,Smad3,p-Smad2,and p-Smad3(P＜0.05).Relative to the model group,the TGF-β1+ORI group demonstrated a signifi-cant downregulation in the expression of NLRP3,ASC,Smad2,Smad3,p-Smad2,and p-Smad3(P＜0.05).Conclusion ORI the proliferation,migration,and invasiveness of HKF,as well as the formation and deposition of the extracellular matrix,through the blockade of the TGF-β1/Smad signaling pathway and the NLRP3-mediated in-flammatory response.