The pulp from lychee, a tropical to subtropical fruit, contains large quantities of phenolic compounds and exhibits antioxidant activities both in vitro and in vivo. In the present study, we investigated the mechanisms underlying the hepatoprotective effects of lychee pulp phenolics (LPPs) against restraint stress-induced liver injury in mice. After 18 h of restraint stress, increased levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were observed. High levels of thiobarbituric acid reactive substances (TBARS) were also found. Restraint stress causes liver damage, which was protected against by LPP pretreatment at a dosage of 200 mg (kg d)(-1) for 21 consecutive days. This treatment remarkably decreased the serum ALT, AST and TBARS levels, elevated the liver glutathione (GSH) content, and the activities of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT). Furthermore, respiratory chain complex and Na(+)-K(+)-ATPase activities were enhanced in liver mitochondria, while mitochondrial membrane potential levels and reactive oxygen species (ROS) production decreased. Thus, treatment with LPPs ameliorated restraint stress-induced liver mitochondrial dysfunction. These results suggest that LPPs protect the liver against restraint stress-induced damage by scavenging free radicals and modulating mitochondrial dysfunction. Thus, lychee pulp may be a functional biofactor to mitigate oxidative stress.
Sensitive
detection of alkaline phosphatase (ALP) activity in human
serum is important for diagnosis of various diseases. In this work,
a novel sandwich-structured upconversion nanoparticle, NaYF4:Yb/Er@NaErF4@NaYF4, is fabricated to construct
an upconversional nanoprobe for ultrasensitive detection of phosphate
and ALP activity. The inner shell of NaErF4 bridges the
emitters in the core with the external luminescence quenchers to greatly
improve the energy transfer efficiency. The quencher, herein, is a
coordination complex formed between sulfosalicylic acid and ferric
ions. Owing to the higher affinity for phosphate, ferric ions dissociate
from the complex and potently combine with phosphate ions, thus interrupting
the energy transfer process and recovering the luminescence. This
upconversional nanoprobe shows rapid and sensitive detection of phosphate
with a limit of detection of 2.5 nM. Because ALP catalyzes the hydrolysis
of p-nitrophenyl phosphate to form p-nitrophenol and inorganic phosphate ions, the nanoprobe is further
utilized to achieve sensitive detection of ALP with a limit of detection
of 0.5 μU/mL. This novel strategy offers a new opportunity for
developing sensitive upconversional nanoprobes and many other energy
transfer-based applications.
Based on many studies, trichosanthin (TCS) has an antiviral effect that regulates immune response, and targets cancer cells to exert broad-spectrum anti-tumor pharmacological activities. It is speculated that TCS may be a potential natural active drug for preventing as well as treating cervical cancer. But the clearer impact along with underlying TCS mechanism on cervical cancer are still unclear. The purpose of this study is to investigate the function and potential mechanism of TCS in cervical cancer. We measured the viability of cervical cancer cell lines (HeLa & caski cells) using CCK-8 analysis, detected cell proliferation efficiency through Ki-67 staining, analyzed cell apoptosis rate via flow cytometry as well as annexin V-FITC/PI double staining, performed apoptosis-related protein expression through western blotting, evaluated cell migration along with invasion by wound as well as transwell assays, carried out MMP via JC-1 and Rh123 fluorescent probes, as well as detected intracellular ATP and ROS levels by flow cytometry, respectively, to evaluate the effects of TCS. We found that TCS inhibited viability along with proliferation, induced apoptosis, as well as inhibited HeLa & caski cell migration along with invasion in a time-and dose-dependent manner. Additionally, TCS also reduced MMP, and the production of adenosine triphosphate, as well as induced the increase of intracellular reactive oxygen species in cancer cell lines. In accordance with the present studies, TCS inhibits HeLa & caski cell proliferation along with migration but promotes their apoptosis, which may be mediated by regulating oxidative stress.
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