Analysis of the Improvement Effect of Nervonic Acid Extracted from Xanthoceras Sorbifolium Bunge Oil on Antioxidant Response and Inflammatory Response in Parkinson's Disease.

OBJECTIVE: An extract of Xanthoceras sorbifolium Bunge (XSB) oil called nervonic acid (NA) was studied for its potential to ameliorate oxidative stress and inflammation in people living with Parkinson's disease (PD). Recrystallization column chromatography was performed to isolate NA from the XSB oil. Twenty-five C57BL/6 mice (8-10 weeks old) were randomly assigned to one of five groups (control, model, low, medium, and high dosage). METHODOLOGY: Except for the control group, all of the experimental animals received an intraperitoneal injection of 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The next phase was administering varied doses of NA produced from XSB oil to mice. Control, model, low-dose, medium-dose, and high-dose groups were created at random from SH-SY5Y and PC-12 cell cultures. Our study's control groups exhibited typical normative conduct. RESEARCH: Polymerase chain reaction (PCR) was used to examine oxidative stress (OS) and inflammatory factors (IFs) in cells. By the time recrystallization column chromatography had finished its analysis, the concentration of NA had increased by a factor of roughly 26. RESULTS: The model and high-dose groups showed similar levels of apoptosis in behavior (p > 0.05). All three NA treatment groups showed decreases in IFs and increases in superoxide dismutase (SOD) and GSH-Px mRNA (p < 0.05). NA, an antioxidant and anti-inflammatory chemical, has shown promising results in PD animal and cell models. CONCLUSIONS: NA synthesized from XSB oil will soon be available for use in the treatment of Parkinson's disease. With the use of deep learning, patients will be able to arrest their health deterioration and enjoy an improved standard of living.

Berberine Inhibits Herpes Simplex Virus 1 Replication in HEK293T Cells.

Berberine exhibits polytrophic medicinal roles in various diseases and is safe and effective. However, its role and the underlying mechanism in the replication of herpes simplex virus 1 (HSV-1) remain unreported. This research aimed to determine the functional mechanisms of berberine on HSV-1 infection. We determined the CC50 (405.11 ± 15.67 µM) and IC50 (45.6 ± 6.84 µM) of berberine on HEK293T cells infected with HSV-1. Berberine inhibited the transcription and translation of HSV-1 activity-related genes (gD, ICP-4, ICP-5, and ICP-8) in HSV-1-infected HEK293T cells dose-dependently. Berberine also inhibited the phosphorylation of MAPK proteins (JNK and p38) and inflammatory responses induced by HSV-1 infection in HEK293T cells dose-dependently. In conclusion, berberine attenuates HSV-1 replication through its activity, infective ability, and inflammatory response. Our research indicated that berberine may be a candidate drug for HSV-1 infection.

Nervonic acid amends motor disorder in a mouse model of Parkinson's disease.

[This retracts the article DOI: 10.1515/tnsci-2020-0171.].

Nervonic acid amends motor disorder in a mouse model of Parkinson's disease.

OBJECTIVES: Parkinson's disease (PD) is a kind of common neurodegenerative disease in the world. Previous studies have proved that nervonic acid (NA), extracted from Xanthoceras sorbifolia Bunge, has the potentials of neuroprotection. However, the effect of NA on the PD remained unknown. This study was designed to investigate the NA's potential function and relative mechanism on motor disorder. METHODS: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used for producing parkinsonism motor disorder on male C57BL/6 mice. Toxicity experiments and behavioral assay were performed to evaluate the effect of NA. Besides, the expression levels of tyrosine hydroxylase and α-synuclein, as well as striatal dopamine (DA), serotonin, and their metabolites were explored through immunoblotting and chromatography after NA treatment in vivo. RESULTS: We found that NA could alleviate the MPTP-induced behavioral deficits dose-dependently. Moreover, NA has no toxic effects on the mouse liver and kidney. Of note, we found that NA significantly reduced the impact of MPTP impairment and striatal DA, serotonin, and metabolites were remained unaffected. In addition, tyrosine hydroxylase was upregulated while α-synuclein being downregulated and the oxidative stress was partially repressed evidenced by the upregulation of superoxide dismutase and glutathione activity after NA treatment. CONCLUSION: Our findings unveil NA's potential for protecting motor system against motor disorder in the PD mouse model without any side effects, indicating NA as an alternative strategy for PD symptom remission.