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Objective: This retrospective study aimed to investigate the association between TNs and the systemic immune-inflammation index (SII) and the aggregate index of systemic inflammation (AISI) in patients with T2DM. Methods: A total of 370 T2DM patients, who were admitted to Dongzhimen Hospital between January 2020 and March 2023, were included in this retrospective study. Binary logistic regression models with multivariable adjustment were employed to assess the relationship between SII, AISI quartiles, and TNs. Furthermore, receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic accuracy of SII and AISI in identifying T2DM patients with TNs. Results: Age, diabetes duration, diabetic nephropathy (DN), SII, and AISI demonstrated significant positive associations with TNs. Compared to the first quartile of SII, the second, third, and fourth quartiles showed increased risks of TNs with hazard ratios (HRs) of 1.578 (0.883–2.820), 2.279 (1.257–4.131), and 3.626 (1.931–6.810), respectively (P < 0.001). Similar results were observed for AISI and TNs. ROC curve analysis revealed that SII and AISI exhibited a high discriminatory capability for identifying TNs in the overall and male participant group, whereas the significance among females was not discernible. Conclusions: This study provides evidence that SII and AISI are independent risk factors for TNs, suggesting that elevated SII and AISI levels may contribute to the development of TNs in patients with T2DM particularly among male individuals. [ABSTRACT FROM AUTHOR]

[Display omitted] • Novel 25 dehydroabietic acid derivatives. • D1 shows the strongest relaxation effect in vitro and in vivo. • D1 has multi-targets effect. Using dehydroabietic acid as the lead compound for structural modification, 25 dehydroabietic acid derivatives were synthesized. Among them, compound D1 not only showed the strongest relaxation effect on the aortic vascular ring in vitro (Emax = 99.5 ± 2.1%, EC 50 = 3.03 ± 0.96 µM), but also significantly reduced systolic and diastolic blood pressure in rats at a dose of 2.0 mg/kg in vivo. Next, the vascular protective effect of the best active D1 and its molecular mechanism were further investigated by HUVECs. The results showed that D1 induced endothelium-dependent diastole in the rat thoracic aorta in a concentration-dependent manner. Endothelium removal or aortic ring pretreatment with NG-nitro- l -arginine methylester (l -NAME), 1 H -[1,2,4]-oxadiazolo-[4,3-a]-quinoxalin-1-one (ODQ), and tetraethylammonium (TEA) significantly inhibited D1 -induced relaxation. In addition, wortmannin, KT5823, triciribine, diltiazem, BaCl 2 , 4-aminopyridine, indomethacin, propranolol, and atropine attenuated D1 -induced vasorelaxation. D1 increased the phosphorylation of eNOS in HUVECs Furthermore, D1 attenuated the expression of TNF-α-induced cell adhesion molecules such as ICAM-1 and VCAM-1. However, this effect was attenuated by the eNOS inhibitors l -NAME and asymmetric dimethylarginine (ADMA). The findings suggest that D1 -induced vasorelaxation through the PI3K/Akt/eNOS/NO/cGMP/PKG pathway by activating the K Ca , K ir and K V channels or muscarinic and β-adrenergic receptors, and inhibiting the l -type Ca2+ channels, which is closely related to the hypotensive action of the agent. Furthermore, D1 exhibits an inhibitory effect on vascular inflammation, which is associated with the observed vascular protective effects. [ABSTRACT FROM AUTHOR]

[Display omitted] • MgIG mitigated LPS-induced liver damage by inhibiting apoptosis and inflammation. • MgIG increased the expression of IL-22 in LPS-induced mice. • MgIG inhibited TLR4/NF-κB pathways and induced autophagy in LPS-treated mice. • MgIG has hepatoprotective effects partially by IL-22-activated autophagy. Liver disease has become a major cause of premature mortality worldwide. It is well known that dysregulated inflammation response plays a crucial role in most liver diseases. As a Chinese medicinal herb, Magnesium isoglycyrrhizinate (MgIG) has been proven to have good hepatoprotective activity and has been used in clinic to treat liver disease. However, the mechanisms by which MgIG regulates LPS-induced liver injury and inflammation in vivo remain elusive. In our study, MgIG pretreatment mitigated LPS-induced liver damage by suppressing apoptosis and inflammation via regulating macrophage/neutrophil infiltration. MgIG ameliorated the effects of LPS on pro-oxidant enzymes (NOX1/2/4) and anti-oxidant enzymes (SOD1/2). Interestingly, we found that the level of the hepatoprotective cytokine interleukin (IL)–22 was significantly upregulated in MgIG-treated liver tissues, which might be a potential mechanism of MgIG against liver injury. Moreover, we found that MgIG treatment not only inhibited TLR4/MyD88/NF-κB signaling pathway, but also activated autophagy. Furthermore, IL-22 treatment activated autophagy and inhibited TLR4/NF-κB signaling pathway in vitro , suggesting that IL-22-activated autophagy and -inhibited inflammation also participated in the protective effects of MgIG. Altogether, our results uncovered the potential mechanisms of the hepatoprotective effects of MgIG, which provided critical evidence to support the use of MgIG to prevent and treat liver diseases. [ABSTRACT FROM AUTHOR]

Although oral probiotics can improve breast microecology and alleviate the inflammatory response, there are no data regarding cases with existing abscesses. We aimed to investigate the effect of Lactobacillus fermentum CECT5716 during needle aspiration in patients with lactational breast abscesses. Patients (aged 20–41 years) with lactational single-cavity breast abscesses (diameter 3–6 cm) from 12 hospitals were randomly assigned to the experimental (n = 51) and control groups (n = 50). Outcome measures included the abscess cure rate on treatment day-5, delactation rate, relieving pain rate, and number of needle aspirations until day-28. The experimental group's 5-day cure rate (43.1%) was significantly higher (p < 0.05). Breastfeeding continuation on day-5 did not differ significantly (experimental group: 88.2%, control group: 96.0%, p = 0.269). In the experimental and control groups, 19.6% and 14.0% of patients experienced moderate to severe pain on day-5, respectively, with no statistically significant differences (p = 0.451). Four patients in each group developed diarrhea, with adverse reaction rates of 7.84% and 8.0%, respectively. No adverse reactions were reported in the infants. L. fermentum can shorten the healing time in patients with lactational breast abscesses. Trial registration This study was registered in the Chinese Clinical Trial Registry (http://www.chictr.org.cn), registration number: ChiCTR2000032682, registration date: 6/May/ 2020; first entry date: 11/May/2020. [ABSTRACT FROM AUTHOR]

Objective To examine whether curcumin has protective effect on insulin resistance induced by bisphenol A (BPA) in LO2 cells and whether this effect was mediated by inhibiting the inflammatory mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) pathways. Methods LO2 cells were stimulated with BPA in the presence or absence of curcumin for 5 days. Glucose consumption, activation of insulin signaling, MAPKs and NF-κB pathways, levels of inflammatory cytokines and MDA production were analyzed. Results Curcumin prevented BPA-induced reduction of glucose consumption and suppression of insulin signaling pathway, indicating curcumin alleviated BPA-triggered insulin resistance in LO2 cells. mRNA and proteins levels of TNF-α and IL-6, as well as MDA level in LO2 cells treated with BPA were decreased by curcumin. Furthermore, curcumin downregulated the activation of p38, JNK, and NF-κB pathways upon stimulation with BPA. Inhibition of JNK pathway, but not p38 nor NF-κB pathway, improved glucose consumption and insulin signaling in BPA-treated LO2 cells. Conclusion Curcumin inhibits BPA-induced insulin resistance by suppressing JNK pathway. [ABSTRACT FROM AUTHOR]