Interaction between the left ventricular ejection fraction and left ventricular strain and its relationship with coronary stenosis.

BACKGROUND: Coronary artery stenosis (CAS) is the most common type of heart disease and the leading cause of death in both men and women globally. CAS occurs when the arteries that supply blood to the heart muscle harden and become narrower due to plaque buildup - cholesterol and other material - on their inner walls. As a result, the heart muscle cannot receive the blood or oxygen it needs. Most heart attacks happen when a blood clot suddenly cuts off the hearts' blood supply, causing permanent heart damage. AIM: To analyze the relationship between the left ventricular ejection fraction (LVEF), left ventricular strain (LVS), and coronary stenosis. METHODS: A total of 190 participants were enrolled in this trail. The control group comprised 93 healthy individuals, and observation group comprised 97 patients with coronary heart disease who were hospitalized between July 2020 and September 2021. Coronary lesions were assessed using the Gensini score, and the LVEF and LVS were measured using magnetic resonance imaging (MRI). The interaction between the LVEF and LVS was examined using a linear regression model. The relationship between LVEF and coronary stenosis was examined using Spearman's correlation. RESULTS: The LVEF of the observation group was lower than that of the control group. The left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV) of the observation group were significantly higher than those of the control group (P < 0.05). The longitudinal and circumferential strains (LS, CS) of the observation group were significantly higher than those of the control group; however, the radial strain (RS) of the observation group was significantly lower than that of the control group (P < 0.05). LVS, LS, and CS were significantly negatively correlated with the LVEF, and RS was positively correlated with the LVEF. There were significant differences in the LVEF, LVESV, and LVEDV of patients with different Gensini scores; the LVEF significantly decreased and the LVESV and LVEDV increased with increasing Gensini scores (P < 0.05). In the observation group, the LVEF was negatively correlated and the LVESV and LVEDV were positively correlated with coronary stenosis (P < 0.05). CONCLUSION: The LVEF measured using MRI is significantly linearly correlated with LVS and negatively correlated with coronary stenosis.

Curcumin Protects against 1-Methyl-4-phenylpyridinium Ion- and Lipopolysaccharide-Induced Cytotoxicities in the Mouse Mesencephalic Astrocyte via Inhibiting the Cytochrome P450 2E1.

Curcumin is extracted from the rhizomes of the ginger family plant Curcuma longa L., which has a good protection for liver, kidney, and immune system. However, there is little information about its contribution in protection of astrocytes recently. The present study was undertaken to elucidate the protective effect of curcumin, an herbal antioxidant, on 1-methyl-4-phenylpyridinium ion- (MPP(+)-) and lipopolysaccharide- (LPS-) induced cytotoxicities, as well as the underlying mechanisms by using primary mouse mesencephalic astrocytes. The results showed that curcumin protected the mesencephalic astrocytes from MPP(+)- and LPS-induced toxicities along with reducing reactive oxygen species (P < 0.05) and maleic dialdehyde (P < 0.05) sufficiently. Moreover, curcumin significantly inhibited the cytochrome P450 2E1 (CYP2E1) expression (P < 0.01 at mRNA level, P < 0.05 at protein level) and its activity (P < 0.05) sufficiently induced by MPP(+) and LPS in the mouse mesencephalic astrocytes. And curcumin as well as diallyl sulphide, a CYP2E1 positive inhibitor, ameliorated MPP(+)- and LPS-induced mouse mesencephalic astrocytes damage. Accordingly, curcumin protects against MPP(+)- and LPS-induced cytotoxicities in the mouse mesencephalic astrocyte via inhibiting the CYP2E1 expression and activity.

Down regulation of differentiated embryonic chondrocytes 1 (DEC1) is involved in 8-methoxypsoralen-induced apoptosis in HepG2 cells.

8-Methoxypsoralen (8-MOP), a naturally occurring compound, is a potent modulator of epidermal cell growth and differentiation in combination with ultraviolet light. However, there is little information on 8-MOP contribution to cell apoptosis alone. In the study, we evaluated 8-MOP, independently of its photoactivation, induced apoptosis in human hepatocellular carcinoma HepG2 cells. And we provide a molecular explanation linking 8-MOP to induce apoptosis. In HepG2 cells, treatment with 8-MOP induced the cell apoptosis in both dose-dependent and time-dependent manners. IC(50) values of 8-MOP were 8.775, 5.398 µM for 48 and 72 h, respectively. Further study showed that 8-MOP decreased the procaspase-3, procaspase-8, and procaspase-9, increased the ratio of Bax/Bcl-2 and decreased the survivin. Moreover, 8-MOP decreased differentiated embryonic chondrocyte gene1 (DEC1). Overexpression of DEC1 antagonized partially apoptosis induced by 8-MOP. And overexpression of DEC1 abolished the decrease of survivin and the activation of caspase-3 induced by 8-MOP partially. So, down regulation of DEC1 is involved in 8-MOP-induced apoptosis in HepG2 cells. Here, it is demonstrated that DEC1 possesses anti-apoptotic effects in 8-MOP-treated HepG2 cells. The findings provide more of a basis for 8-MOP as an anti-tumor agent in cancer therapy.