Application of Levosimendan in Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection Patients with Myocardial Injury.

Objective: This study aims to investigate the effectiveness of levosimendan in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection complicated by cardiac insufficiency and myocardial injury. Methods: A total of 22 patients with SARS-CoV-2 infection and myocardial injury, admitted to the Cardiology Department of our hospital between December 2022 and February 2023, are randomly divided into two groups: a dobutamine general treatment group and a levosimendan observation treatment group. The treatment outcomes of the two groups are compared and analyzed. Results: The overall improvement rate in the general treatment group is 80%, while the levosimendan treatment group shows a 100% improvement rate. There is a statistically significant difference between the two groups (P < .05). Post-treatment, the left ventricular ejection fraction for the general treatment group and the levosimendan treatment group are (48 ± 7)% and (54 ± 6)%, respectively. Additionally, the left ventricular end-diastolic diameter is (55.0 ± 3.0) mm in the general treatment group and (51 ± 5.0) mm in the levosimendan group, with a statistically significant difference (P < .05). After active treatment, the plasma levels of B-type natriuretic peptide (Brain Natriuretic Peptide, NT-proBNP) are significantly lower in the levosimendan treatment group than in the general treatment group (P < .05). Moreover, the plasma levels of interleukin-6 (IL-6) and C-reactive protein (CRP) in the levosimendan group decrease slightly faster than those in the general treatment group, with a statistically significant difference (P < .05). The length of hospital stay in the levosimendan group is (12 ± 3) days, significantly lower than the general treatment group (16 ± 5) days, with a statistically different result (P < .05). Conclusions: Levosimendan demonstrates significant efficacy in patients with novel coronavirus infection complicated by myocardial injury, resulting in improved clinical symptoms, enhanced cardiac function, shorter hospital stays, early discharge, and cost savings.

Overexpression of the bioactive lunasin peptide in soybean and evaluation of its anti-inflammatory and anti-cancer activities in vitro.

Lunasin, a bioactive peptide with a variety of physiological functions, was overexpressed in soybean to generate a transgenic soybean. Polymerase chain reaction (PCR) analysis suggested that lunasin was successfully inserted into the soybean genome, and three transgenic lines, L12, L43, and L45, were selected for further study. Lunasin expression was characterized in the lines by Western blot and ultra-performance liquid chromatography with tandem mass spectrometry. Enzyme-linked immunosorbent assay showed that lunasin content in L12, L43, and L45 lines was 1.47 mg g-1, 1.32 mg g-1 and 1.98 mg g-1, respectively; these values were significantly higher than that in wild-type soybean (0.94 mg g-1). Lunasin enrichments from transgenic soybean (LET) exhibited stronger DPPH, ABTS+, and oxygen radical scavenging activity than lunasin enrichments from wild-type soybean (LEW). Further, LET presented superior anti-inflammatory activity on lipopolysaccharide-induced macrophage cells compared to LEW, and it significantly suppressed the release of nitric oxide (NO) and pro-inflammatory cytokines including interleukin-1 and -6. Moreover, LET showed higher anti-proliferation activity on MDA-MB-231 cells than LEW. Immunofluorescence staining showed that LET could internalize into NIH-3T3 cells, and localize in the nucleus. In conclusion, it is feasible and efficient to produce lunasin through a transgenic soybean expression system. Lunasin overexpressing soybean could be consumed as a functional food in the diets of patients with cancer and obesity in the future.

The S-nitrosylation status of PCNA localized in cytosol impacts the apoptotic pathway in a Parkinson's disease paradigm.

It is generally accepted that nitric oxide (NO) or its derivatives, reactive nitrogen species (RNS), are involved in the development of Parkinson's disease (PD). Recently, emerging evidence in the study of PD has indicated that protein S-nitrosylation triggers the signaling changes in neurons. In this study, SH-SY5Y cells treated with rotenone were used as a model of neuronal death in PD. The treated cells underwent significant apoptosis, which was accompanied by an increase in intracellular NO in a rotenone dose-dependent manner. The CyDye switch approach was employed to screen for changes in S-nitrosylated (SNO) proteins in response to the rotenone treatment. Seven proteins with increased S-nitrosylation were identified in the treated SH-SY5Y cells, which included proliferating cell nuclear antigen (PCNA). Although PCNA is generally located in the nucleus and participates in DNA replication and repair, significant PCNA was identified in the SH-SY5Y cytosol. Using immunoprecipitation and pull-down approaches, PCNA was found to interact with caspase-9; using mass spectrometry, the two cysteine residues PCNA-Cys81 and -Cys162 were identified as candidate S-nitrosylated residues. In addition, the evidence obtained from in vitro and the cell model studies indicated that the S-nitrosylation of PCNA-Cys81 affected the interaction between PCNA and caspase-9. Furthermore, the interaction of PCNA and caspase-9 partially blocked caspase-9 activation, indicating that the S-nitrosylation of cytosolic PCNA may be a mediator of the apoptotic pathway.