Lactobacillus plantarum ZJ316 improves the quality of Stachys sieboldii Miq. pickle by inhibiting harmful bacteria growth and degrading nitrite, promoting the gut microbiota health in vitro

Microbial contamination and nitrite accumulation are two major concerns on the quality control of fermented vegetables. In the present study, a lactic acid bacteria strain Lactobacillus plantarum ZJ316 (ZJ316) was...

Stachys sieboldii Miq. Root Attenuates Weight Gain and Dyslipidemia in Rats on a High-Fat and High-Cholesterol Diet

This study aimed at investigating the anti-obesity and anti-dyslipidemic effects of Stachys sieboldii Miq. root (SS) powder in rats following a high-fat and high-cholesterol (HFC) diet for 6 weeks. Thirty-two Sprague–Dawley rats were fed one of the following diets: a regular diet (RD), HFC, HFC supplemented with 3% SS (HFC + 3SS) or HFC supplemented with 5% SS (HFC + 5SS). Following an HFC diet increased body weight (BW) gain (p < 0.001) and the food efficiency ratio (FER; p < 0.001); however, SS consumption gradually prevented the HFC-induced BW gain (p < 0.001) and increase in FER (p < 0.01). The HFC diet resulted in increased liver size (p < 0.001) and total adipose tissue weight (p < 0.001), whereas the SS supplementation decreased hepatomegaly (p < 0.05) and body fat mass (p < 0.001). SS consumption prevented the increased activities of serum alanine aminotransferase (ALT; p < 0.001), aspartate aminotransferase (AST; p < 0.001), alkaline phosphatase (ALP; p < 0.01 in HFC + 5SS) and lactate dehydrogenase (LDH; p < 0.001 in HFC + 5SS) induced by the HFC diet (p < 0.001). The SS supplementation improved lipid profiles in the circulation by lowering triglyceride (TG; p < 0.01), total cholesterol (TC; p < 0.001) and non-HDL cholesterol (non-HDL-C; p < 0.001) levels, as well as the atherogenic index (p < 0.01) and cardiac risk factor (p < 0.01). The lipid distribution in the liver (p < 0.05) and white adipose tissues (WAT; p < 0.001) of the HFC + SS diet-consuming rats was remarkably lower than that of the HFC diet-consuming rats. The average size of the epididymal adipose tissue (p < 0.001) was significantly lower in the HFC + SS diet-fed rats than in the HFC diet-fed rats. The fecal lipid (>3% SS; p < 0.001) and cholesterol (5% SS; p < 0.001) efflux levels were significantly elevated by the SS supplementation compared to those measured in the RD or HFC diet-fed groups. In addition, the hepatic lipid and cholesterol metabolism-related gene expressions were affected by SS consumption, as the hepatic anabolic gene expression (Acc; p < 0.001, Fas; p < 0.001 and G6pdh; p < 0.01) was significantly attenuated. The HFC + 5SS diet-fed rats exhibited elevated hepatic Cyp7a1 (p < 0.001), Hmgcr (p < 0.001) and Ldlr (p < 0.001) mRNA expression levels compared to the HFC diet-fed rats. These results suggest that SS may possess anti-adipogenic and lipid-lowering effects by enhancing lipid and cholesterol efflux in mammals.

Antiproliferative Properties of Extracts from Stachys sieboldii MIQ

Background: The objective of this study was to investigate the antiproliferative effect of Stachys sieboldii MIQ. extracts on cancer cell lines. Methods: Dried S. sieboldii MIQ. was extracted using acetone/methylene chloride (A+M) or methanol (MeOH), and then fractionated using n-hexane, 85% aq. methanol (MeOH), butanol (BuOH) and distilled water. The cytotoxic activity of S. sieboldii MIQ. against AGS human gastric, HT-29 human colon and HT-1080 fibroblast cancer cell lines was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. Results: The A+M extract showed significantly higher inhibition of cell growth in all three cell lines compared to the MeOH extract (p < 0.05). All the extracts and fractions from S. sieboldii MIQ. decreased the growth of AGS cells, and the effect was concentration-dependent. Among the different fractions, the n-Hexane and 85% aq. MeOH fractions inhibited AGS cell growth by >50% at a concentration of 0.1 mg/mL (p < 0.05). All fractions inhibited the proliferation of HT-29 cancer cell lines (p < 0.05), showing >50% inhibition at a concentration of 0.25 mg/mL. The A+M extract inhibited the growth of the HT-1080 cancer cells by 60% at a concentration of 0.25 mg/mL. The n-Hexane and 85% aq. MeOH fractions showed the highest growth inhibitory effect on the HT-1080 cancer cells (p < 0.05), similar to that observed in the AGS cancer cells. Conclusion: Thus, the n-Hexane and 85% aq. MeOH fractions from S. sieboldii MIQ. likely contain bioactive compounds such as polyphenols and flavonoids that could prevent cancer proliferation. Further research is needed to isolate these important compounds from the extracts.

Stachys sieboldii Extract Supplementation Attenuates Memory Deficits by Modulating BDNF-CREB and Its Downstream Molecules, in Animal Models of Memory Impairment

Cholinergic dysfunction, impaired brain-derived neurotrophic factor and cAMP response element binding protein (BDNF-CREB) signaling are one of the major pathological hallmarks of cognitive impairment. Therefore, improving cholinergic neurotransmission, and regulating the BDNF-CREB pathway by downregulating apoptosis genes is one strategy for inhibiting the etiology of dementia. This study evaluates the potential effects of Stachys sieboldii MIQ (SS) extract against cognitive dysfunction and its underlying mechanisms. SS supplementation for 33 days improved scopolamine-induced memory impairment symptoms in Morris water maze test and Y-maze test. SS reduced the acetylcholineesterase activity and significantly increase acetylcholine and cholineacetyltransferase activity in the brain. In the subsequent mechanism study, SS regulated the mRNA expression level of neuronal plasticity molecules such as (nerve growth factor) NGF, BDNF, CREB, and its downstream molecules such as Bcl-2 and Egr-1 by downregulating the neuronal apoptosis targets in both hippocampus and frontal cortex. Additionally, inward currents caused by SS in hippocampal CA1 neurons was partially blocked by the GABA receptor antagonist picrotoxin (50 μM), suggesting that SS acts on synaptic/extrasynaptic GABAA receptors. These findings indicate that SS may function in a way that is similar to nootropic drugs by inhibiting cholinergic abnormalities, and neuronal apoptosis targets and ultimately increasing the expression of BDNF-CREB.