Since antediluvian times, the scientific community has realized that natural compounds exhibit enormous potential for the treatment of terrible diseases, such as cancer. Despite a variety of effective bioactive molecules, effective therapies still need to be developed to treat cancer. Hence, it is necessary to study the interactions of natural molecules with their cellular targets. Arctigenin (ATG), a natural lignan compound extracted from Arctium lappa, inhibits the growth of various cancer cells, such as those of the stomach, lungs, liver, and colon, as well as leukocytes, and regulates numerous intracellular activities, such as antioxidative, anti-inflammatory, and anticancer activities. The intention of this paper is to summarize and generally analyse the molecular pathways that are involved in the anticancer effects of ATG. In addition, the interactions of ATG with other drugs are also highlighted in this paper.

In the past few decades, intracellular calcium overload has been shown to induce cell death through multiple signaling pathways. In this study, we used BAPTA-AM, a well-known membrane-permeable Ca2+ chelator, to prevent cell injury by allaying the intracellular calcium overload. We explored the clinical potentials of BAPTA-AM-loaded liposome (BAL) in the treatment of the acute liver failure (ALF) mouse model, which is characterized by severe hepatic necrosis and apoptosis. We discovered that BAL can significantly inhibit D-GalN-induced LO2 cell damage as it increased cell viability by 60% and downregulated the LPS-stimulated inflammatory response in RAW 264.7 macrophages by reversing the morphological change and modulating TNF-α and NF-κB expressions. Through systemic administration, BAL can rapidly accumulate in damaged liver tissue and exhibit excellent treatment effects on the D-GalN/LPS-induced ALF mouse model, including elevation of the survival rate (from 10 to 80%), recovery of normal liver indexes and liver health indicators, improvement of liver blood microcirculation (increased the blood flow volume by 80% and flow rate by 60%), and blood coagulation. The underlying hepatoprotective effect of BAL is presumably based on the antinecrosis and antiapoptosis abilities attributed to its inhibition on oxidative stress, restriction on TNF-α receptor, and mitochondria-mediated apoptotic pathway by effectively clearing the overloaded intercellular calcium. BAL holds great potential as a new therapeutic strategy for ALF treatment, and its prominent cell rescue ability provides ample opportunities for the treatment of many other diseases that are characterized by rapid and massive cell damage.

Rationale: Extensive off-label use may affect the safety profile of tigecycline. Tigecycline-associated hypofibrinogenemia is potentially life threatening, although the frequency of life-threatening reactions is unknown and their incidence is easily overlooked. We report a case of 2 instances of treatment with high-dose tigecycline, each of which presented with hypofibrinogenemia. Patient concerns: An 86-year-old male patient was treated twice with high-dose tigecycline and presented with hypofibrinogenemia both times. The decrease in fibrinogen occurred within 3 to 7 days of tigecycline treatment. Other coagulation parameters had slightly prolonged values. Diagnoses: Coagulopathy and hypofibrinogenemia. Interventions: We discontinued the tigecycline. Outcomes: The fibrinogen level normalized within 5 days after the withdrawal of tigecycline. Following 80 days of hospitalization, the patient was transferred to the rehabilitation hospital for further treatment. Lessons: We suggest routine strict monitoring of coagulation parameters, particularly fibrinogen. Attention should be paid to below-normal fibrinogen levels due to increased bleeding risk and severity of reaction at fibrinogen levels below 1 g/L.

Background. L-carnitine mediates the utilization of fatty acids and glucose in the myocardium. The potential of L-carnitine in managing dilated cardiomyopathy (DCM) in patients has been extensively reported, with additional benefits. Objective. This meta-analysis purposed to explore the clinical efficacy of L-carnitine therapy on DCM patients. Methods. We searched publications up to May 2020 from several databases including PubMed, Embase, Cochrane Library, Chinese Biomedical (CBM) database, Chinese Science and Technology Periodicals database (VIP), Chinese National Knowledge Infrastructure (CNKI) database, and Wanfang database. Subsequently, publications that met the inclusion criteria were systematically evaluated by two independent reviewers. Results. A total of 23 RCTs conducted in China with 1455 DCM patients were included in this study. In the meta-analysis, L-carnitine therapy was associated with a considerable improvement in the overall efficacy ( RR = 1.28 , 95% CI (1.21-1.36), P < 0.0001 ), left ventricular ejection fraction (LVEF) ( MD = 6.16 % , 95% CI (4.50, 7.83), P < 0.0001 ), and cardiac output (CO) ( MD = 0.88  L/min, 95% CI (0.51, 1.25), P < 0.0001 ) as compared to the control group. Moreover, L-carnitine therapy significantly decreased left ventricular end-diastolic dimension (LVEDD) ( MD = − 2.53 , 95% CI (-3.95, -1.12), P = 0.0005 ), brain natriuretic peptide (BNP) ( SMD = − 1.71  ng/L, 95% CI (-3.02, -0.40), P = 0.01 ), and the transforming growth factor-beta (TGF-β1) ( MD = − 56.78  ng/L, 95% CI (-66.02, -47.53), P < 0.0001 ). Conclusions. L-carnitine potentially enhanced the therapeutic efficiency in DCM patients. Following weaknesses in the evidence due to low methodological quality and high clinical heterogeneity in the included studies, well-designed trials are recommended.