ABSTRACT
Mori Cortex is the dry root bark of Moras alba L. and usually used in clinical practice. It is sweet and cold in nature, and enters the lung meridian. With effects in purging lung and relieving asthma, and inducing diuresis to reduce edema, it is mainly used to treat lung heat, asthma, cough, swelling, urine deficiency and facial skin edema. In clinic, it is mainly used for the treatment of respiratory system, urinary infection and diabetes mellitus. In recent years, great progress has been made in studies on the pharmacological effects of Mori Cortex. The literatures on the pharmacological effects of Mori Cortex in recent years were reviewed and summarized in this paper. Mori Cortex has antitussive, anti-inflammatory, hypoglycemic, cardiovascular, antiviral, anticancer, immunoregulatory, antioxidation and anti-allergy and other pharmacological effects, in addition to antitussive, expectorant, antiasthmatic and other traditional effects. Total flavones have a strong pharmacological activity. These extended studies provide valuable reference for the further development of Mori Cortex. This paper summarizes the pharmacological effects of Mori Cortex, proposes the key directions of further studies, and provides the beneficial reference for better development and utilization of Mori Cortex.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of semen-derived enhancer of virus infection (SEVI) on the infection of transmitted/founder (TF) HIV-1 and its matched chronic control (CC) viruses and the antagonism of ADS-J1 on SEVI-mediated enhancement of TF and CC virus infection in vitro.</p><p><b>METHODS</b>PAPself-assembling into SEVI amyloid fibrils was validated by ThT assay. We generated the virus stocks of TF and CC virus pair. TZM-bl cells were infected with the mixture of SEVI and TF or CC viruses for 72 h. Luciferase activity was used to observe the enhancement of SEVI. SEVI was treated with different concentrations of ADS-J1 and incubated with TF or CC viruses. TZM-bl cells were then infected with the mixture and luciferase activity was detected 72 h after infection to analyze the antagonism of ADS-J1 on the enhancing effect of SEVI. ADS-J1 was also incubated with TF and CC viruses directly and TZM-bl cells were infected for 72 h to evaluate the antiviral effect using luciferase assay. SEVI was treated with ADS-J1 and Zeta potential was determined to explore the antagonistic mechanism of ADS-J1.</p><p><b>RESULTS</b>ThT assay showed that PAPwas capable of self-assembly into SEVI amyloid fibrils. SEVI significantly accelerated TF and CC viruses infection (P<0.05), and ADS-J1 not only significantly antagonized the enhancement of SEVI (P<0.05) but also directly inhibited the infection of TF and CC viruses (P<0.05). ADS-J1 neutralized the positive charge of SEVI in a dose-dependent manner.</p><p><b>CONCLUSIONS</b>SEVI promotes the infection of TF and CC strains, and ADS-J1 antagonizes SEVI-mediated enhancement of TF and CC viruses by neutralizing the positive charge of SEVI.</p>