Notes

Cyanine Conjugate-Based Biomedical Imaging Probes.
CD24, CD44, and CD133 expression decreased after SPNs treatment both in PANC-1 spheroid cells and PANC-1 cancer cell line. Under-expression of onco-miRs (miR-21, miR-155, and miR-221), over-expression of several apoptotic potential targets of oncomiRs (Bax, Casp-9, and P53), over-expression of tumor suppressive-miRs (let-7b, miR-34a, and miR-126), and under-expression of Bcl-2 was found in SPNs-treated cells.

We suggest that silybin encapsulated in polymersomes (SPNs) may be useful as a complementary agent for destroying both pancreatic cancer cells and pancreatic CSCs along with chemotherapeutic agents.
We suggest that silybin encapsulated in polymersomes (SPNs) may be useful as a complementary agent for destroying both pancreatic cancer cells and pancreatic CSCs along with chemotherapeutic agents.
Anti-tumor effects of Lactobacilli as normal flora have been described. In a previous study, we identified a protein isolated from the bacterium
ATCC 39392 in acidic pH conditions named metallopeptidase. Therefore, we decided to evaluate the effect of the recombinant plasmid coding metallopeptidase protein on the inhibition, proliferation, or apoptosis of the colorectal and breast cancer cell lines.

Identified metallopeptidase gene of
under the specific colon cancer promoter was transferred to the Human SW480 and MDA-MB231 cells. Cell viability was evaluated in these two cancer cell lines via MTT assay, apoptotic changes, and expression level of p53 and
genes in comparison with healthy blood cells as a control group.

Viability of SW480 and MDA-MB231 cells was identified at 25% and 7%, respectively. An increase in apoptotic cell death in the SW480 cell line was observed as revealed by Tunnel staining. The expression assay of
and
genes showed that MPL protein altered gene expression in a cell type-specific manner. Tunnel analyses showed that the pronounced cytotoxic effect of pEGFP-C2/MPL plasmid on SW480 cells was mediated through apoptosis.

These results suggest that endogenous recombinant MPL under colon specific promoter inhibits the proliferation of SW480 colorectal cancer cells by increase in MAP2K1 and P53 activation.
metallopeptidase under the same circumstances could not affect the growth rate and viability of MDA-MB231 breast cancer cells
.
These results suggest that endogenous recombinant MPL under colon specific promoter inhibits the proliferation of SW480 colorectal cancer cells by increase in MAP2K1 and P53 activation. L. casei metallopeptidase under the same circumstances could not affect the growth rate and viability of MDA-MB231 breast cancer cells in vitro.
Glioblastoma multiforme (GBM), a highly aggressive Grade IV brain tumor, is a significant public health issue due to its poor prognosis and incurability. Neuropeptide substance P (SP) plays a critical role in GBM tumor growth and development via activation of neurokinin-1receptor (NK1R). Moreover, SP is a pro-oxidant factor contributing to oxidative stress in various cell types. However, the link between SP and oxidative stress in cancer cells is not fully investigated. Here, we aimed to identify the effects of SP and NK1R antagonist, aprepitant, on the redox status of GBM cells.

Resazurin assay was employed to determine the effect of aprepitant on viability of U87 glioblastoma cells. 2',7'-dichlorodihydrofluorescein diacetate (H2DCFDA) assay was employed to measure the levels of intracellular reactive oxygen species (ROS). A quantitative real-time polymerase chain reaction was applied to measure the expression of proteins of the thioredoxin system. Commercial kits (ZellBio GmbH) were also used to measure the enzymatic activity of these proteins.

We found that SP increased ROS level in U87 GBM cells, and aprepitant significantly reduced this effect. Furthermore, we found that SP could also affect the thioredoxin system, a central antioxidant enzyme defense system. SP reduced both expression and enzymatic activity of the thioredoxin system's proteins, Trx and thioredoxin reductase (TrxR) and these effects were significantly reduced by aprepitant.

Our results indicated that SP activation of NK1R represented a link between oxidative stress and GBM and highlighted the need for further validations in future studies.
Our results indicated that SP activation of NK1R represented a link between oxidative stress and GBM and highlighted the need for further validations in future studies.
Kaempferide (Ka), a major natural active component of
L, has numerous pharmacological effects such as anti-obesity, anticancer, and anti-hypertension. However, there is no clear evidence that Ka is directly related to inflammation and oxidative stress in obese mice. We aimed to explore the effects of Ka on inflammation and oxidative stress and its mechanism.

The obese mice were induced by a high-fat diet (HFD). The anti-obesity effect was tested by liver and body weight, liver and adiposity index, and white adipose tissue. Blood sample analysis was used to detect the hypolipidemic and hypoglycemic effects. The anti-oxidation effect was assessed using GSH, SOD, MDA, CAT, T-AOC, and other indicators. The anti-inflammatory effect was assessed using TNF-α, MCP-1, and Adiponectin. Western blot and Real-Time PCR were used to evaluate the related signaling pathways.

Obesity, glycolipid metabolism disorder, inflammation, and oxidative stress developed in HFD mice. These changes can be effectively alleviated by Ka treatment for 16 weeks. Further studies have suggested that these beneficial effects of Ka may be associated with inhibition of the TLR4/IκBα/NF-κB signaling pathways.

Ka possesses important anti-obesity, hypoglycemic, and hypolipidemic effects. The mechanism may be causally associated with the TLR4/IκBα/NF-κB signaling pathway, which improves inflammation and oxidative stress.
Ka possesses important anti-obesity, hypoglycemic, and hypolipidemic effects. The mechanism may be causally associated with the TLR4/IκBα/NF-κB signaling pathway, which improves inflammation and oxidative stress.
Since activation of NLRP3 inflammasome results in the production of interleukin-1β (IL 1β) and initiation of inflammation as the key players in development of cancer, this study investigated possible activation of NLRP3 inflammasome during the progression of colorectal cancer (CRC) and evaluated the role of NLRP3 inflammasome in epithelial-mesenchymal transition (EMT) process.

Tissue samples were collected from cancerous (test) and adjacent normal tissues (control) of forty-three male CRC patients (18 grade I and 25 grade III). The gene expression and protein levels were determined by qRT PCR and Western blotting, respectively, and tissue morphological was examined by histopathology.

The gene and protein expression levels of transforming growth factor-β (TGF β), IL 1β, nuclear factor κB (NF κB), NLRP3, and caspase-1, as well as the enzyme activity of caspase-1, were significantly increased in CRC. mRNA and protein levels of TGF-β, mature IL 1β, NF κB, and NLRP3 were higher in patients with grade III. EMRC.
is the bacterium that causes of pulmonary infection among chronically hospitalized patients. Alginate is a common surface antigen of
with a constant structure that which makes it an appropriate target for vaccines. In this study,
alginate was conjugated with to PLGA nanoparticles, and its immunogenicity was characterized as a vaccine.

Alginate was isolated from a mucoid strain of
and conjugated with to PLGA with˝ N-(3-Dimethylaminopropyl)-N'-ethylcarbodiimide hydrochloride ˝= ˝EDAC˝ and N-Hydroxysuccinimide (NHS). Chemical characterization of prepared nano-vaccine was performed using FTIR Spectroscopy, Zetasizer, and Atomic Force Microscopy (AFM). The immunogenicity of this nano-vaccine was evaluated through intramuscular injection into BALB/c mice. Four groups of mice were subjected to the injection of alginate-PLGA, and two weeks after the last administration step, opsonophagocytosis assay, IgG detection, challenge, and cytokine determination via ELISA were carried out.

Alginate-PLGA conjugation was corroborated by FTIR, Zetasizer, and AFM. The ELISA consequence showed that alginate was prospering in the instigation of the humoral immunity.The immunogenicity enhanced against the alginate-PLGA. Remarkably diminished bacterial titer in the spleen of the immunized mice posterior to challenge with PAO1 strain in comparison with the alginate alone and control groups.

The bacterial burden in the spleen significantly decreased after the challenge (
<0.05). The opsonic activity was significantly increased in the alginate- PLGA group (
<0.05).
The bacterial burden in the spleen significantly decreased after the challenge (P less then 0.05). The opsonic activity was significantly increased in the alginate- PLGA group (P less then 0.05).
NMDA glutamatergic receptors are heteromeric receptors with various subunits. GluN2A and GluN3A subunits specify the functional heterogeneity of NMDA receptors. These subunits play a key role in the induction of LTP and synaptic plasticity. Note that, the function of NMDA subunits has interaction with the mechanism of morphine. On the other hand, NeuroAid is a Chinese traditional medicine with neuroprotective and anti-apoptotic effects. In this study, we aimed to investigate the effect of morphine and NeuroAid on expression levels of GluN2A and GluN3A in the hippocampus and striatum of rats.

Morphine sulfate (increasing doses) and NeuroAid (2.5 mg/kg) were injected intraperitoneally. Real-time PCR was used to assess gene expression.

The results showed that morphine increased the expression of GluN2A in the hippocampus and striatum, while NeuroAid increased the expression of both genes in the hippocampus and decreased the expression of GluN3A in the striatum. NeuroAid increased the expression of GluN3A in the hippocampus and GluN2A in the striatum of morphine-addicted rats.

NeuroAid may have interaction with the effect of morphine on glutamatergic neurotransmission; however, this study is innovative and novel, thus, further studies are needed to better understand the effect of NeuroAid and morphine on hippocampal and striatal glutamatergic neurotransmission.
NeuroAid may have interaction with the effect of morphine on glutamatergic neurotransmission; however, this study is innovative and novel, thus, further studies are needed to better understand the effect of NeuroAid and morphine on hippocampal and striatal glutamatergic neurotransmission.
Oxymatrine can regulate glucose metabolism. But the underlying mechanisms remain unclear. We investigated the relationship of oxymatrine and voltage-gated potassium (Kv) channel in rat islet β cells and INS-1 cells.

Insulin secretion and Kv channel currents were tested by radioimmunoassay and patch-clamp technique, respectively. The INS-1 cell viability was detected using cell counting kit-8 experiments. Flowcytometry analysis and western blot were employed for cell apoptosis and protein levels, respectively. INS-1 cell proliferation was assessed by the 5-Ethynyl-2'- deoxyuridine method.

Oxymatrine potentiated insulin secretion at high glucose (
<0.01 vs 11.1 G,
<0.01 vs 16.7 G) and inhibited KV currents at 40 mV (45.73±15.34 pA/pF for oxymatrine, 73.80±19.23 pA/pF for control,
<0.05). After the INS-1 cells were treated with oxymatrine for 12 and 24 hr, KV2.1 channel protein was up-regulated (
<0.01 vs Control). At the same time, compared with the high glucose and high fat group, cell viability and proliferation ability were increased (
<0.
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