Plant-based polyphenol rich protein supplementation attenuated skeletal muscle loss and lowered the LDL level via gut microbiota remodeling in Taiwan's community-dwelling elderly.

Sarcopenia, characterized by muscle loss, negatively affects the elderly's physical activity and survival. Enhancing protein and polyphenol intake, possibly through the supplementation of fermented black soybean koji product (BSKP), may alleviate sarcopenia by addressing anabolic deficiencies and gut microbiota dysbiosis because of high contents of polyphenols and protein in BSKP. This study aimed to examine the effects of long-term supplementation with BSKP on mitigating sarcopenia in the elderly and the underlying mechanisms. BSKP was given to 46 participants over 65 years old with early sarcopenia daily for 10 weeks. The participants' physical condition, serum biochemistry, inflammatory cytokines, antioxidant activities, microbiota composition, and metabolites in feces were evaluated both before and after the intervention period. BSKP supplementation significantly increased the appendicular skeletal muscle mass index and decreased the low-density lipoprotein level. BSKP did not significantly alter the levels of inflammatory factors, but significantly increased the activity of antioxidant enzymes. BSKP changed the beta diversity of gut microbiota and enhanced the relative abundance of Ruminococcaceae_UCG_013, Lactobacillus_murinus, Algibacter, Bacillus, Gordonibacter, Porphyromonas, and Prevotella_6. Moreover, BSKP decreased the abundance of Akkermansia and increased the fecal levels of butyric acid. Positive correlations were observed between the relative abundance of BSKP-enriched bacteria and the levels of serum antioxidant enzymes and fecal short chain fatty acids (SCFAs), and Gordonibacter correlated negatively with serum low-density lipoprotein. In summary, BSKP attenuated age-related sarcopenia by inducing antioxidant enzymes and SCFAs via gut microbiota regulation. Therefore, BSKP holds potential as a high-quality nutrient source for Taiwan's elderly, especially in conditions such as sarcopenia.

Lactobacillus paracasei PS23 Delays Progression of Age-Related Cognitive Decline in Senescence Accelerated Mouse Prone 8 (SAMP8) Mice.

Probiotic supplements are potential therapeutic agents for age-related disorders due to their antioxidant and anti-inflammatory properties. However, the effect of probiotics on age-related brain dysfunction remains unclear. To investigate the effects of Lactobacillus paracasei PS23 (LPPS23) on the progression of age-related cognitive decline, male and female senescence-accelerated mouse prone 8 (SAMP8) mice were divided into two groups (n = 6 each): the control and PS23 groups. From the age of 16 weeks, these groups were given saline and LPPS23, respectively, because SAMP8 mice start aging rapidly after four months of age. After 12 weeks of treatment, we evaluated the effect of LPPS23 by analyzing their appearance, behavior, neural monoamines, anti-oxidative enzymes, and inflammatory cytokines. The PS23 group showed lower scores of senescence and less serious anxiety-like behaviors and memory impairment compared to the control group. The control mice also showed lower levels of neural monoamines in the striatum, hippocampus, and serum. Moreover, LPPS23 induced the anti-oxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx). Higher levels of tumor necrosis factor (TNF)-α and monocyte chemotactic protein-1 (MCP1) and lower levels of interleukin (IL)-10 indicated that LPPS23 modulated the inflammation. Our results suggest that LPPS23 supplements could delay age-related cognitive decline, possibly by preventing oxidation and inflammation and modulating gut⁻brain axis communication.

Taiwanese Green Propolis Ethanol Extract Delays the Progression of Type 2 Diabetes Mellitus in Rats Treated with Streptozotocin/High-Fat Diet.

Taiwanese green propolis ethanol extract (TGPE) is produced only in Taiwan and has a different composition from other types of propolis. TGPE is known for its anti-inflammation, anti-oxidation, and anti-microbial properties, but the effects and mechanisms of TGPE in the modulation of diabetes are unclear. In this study, we investigated the effects of TGPE on type 2 diabetes mellitus (T2DM) in a streptozotocin/high-fat-diet (STZ/HFD)-induced T2DM rat model. The results revealed that TGPE delayed the development and progression of T2DM and reduced the severity of β-cell failure. TGPE also attenuated inflammation and reactive oxygen species ROS in the rats. Moreover, there were higher levels of oxidant cytokines, leptin, and adiponectin in the serum of the TGPE-treated group. Unlike Brazilian propolis, TGPE promoted hepatic genes PPAR-α and CYP7A1, which were related to lipid catabolism and removal. TGPE may thus delay the progression of T2DM through anti-inflammation effects, anti-oxidation effects, and balancing lipid metabolism. It is suggested that TGPE can be a potential alternative medicine for T2DM.

Effects of Lu-Do-Huang Extract (LDHE) on Apoptosis Induction in Human Hep3B Cells.

Lu-Do-Huang (Pracparatum mungo) is a fermented mung bean [corrected] (Vigna radiata) and has long been used as a traditional and functional food in Traditional Chinese Medicine, especially for treating a variety of liver disorders. The present study aimed to evaluate the apoptotic effects of Lu-Do-Huang ethanol extract (LDHE) on Hep3B cells, a human hepatoma cell line. A variety of cellular assays, flow cytometry and immunoblotting were used. Our results showed that LDHE significantly inhibited Hep3B cells growth. Additionally, the cell cycle assay showed that LDHE prevented Hep3B cell entry into S phase and led to an arrest of Hep3B cells in the G0/G1 phase. LDHE induced Hep3B cells to undergo apoptosis as determined through Hep3B cell morphology changes, increase of apoptotic bodies, apoptotic cells, DNA fragmentations and caspase activity. We further examined the protein expression of TRADD, FADD, and Bax to verify the possible apoptotic pathways. The results indicated that LDHE-induced apoptosis in Hep3B cells might be mediated [corrected] by an extrinsic signaling pathway leading to an induction of apoptosis in Hep3B cells. In conclusion, LDHE induced apoptosis and cell cycle arrest in Hep3B cells. Our data provide the evidences regarding the anti-hepatoma potential of LDHE in Hep3B cells.