Exploring the Potential of Crassostrea nippona Hydrolysates as Dietary Supplements for Mitigating Dexamethasone-Induced Muscle Atrophy in C2C12 Cells.

Muscle atrophy is a detrimental and injurious condition that leads to reduced skeletal muscle mass and disruption of protein metabolism. Oyster (Crassostrea nippona) is a famous and commonly consumed shellfish in East Asia and has become a popular dietary choice worldwide. The current investigation evaluated the efficacy of C. nippona against muscle atrophy, which has become a severe health issue. Mammalian skeletal muscles are primarily responsible for efficient metabolism, energy consumption, and body movements. The proteins that regulate muscle hypertrophy and atrophy are involved in muscle growth. C. nippona extracts were enzymatically hydrolyzed using alcalase (AOH), flavourzyme (FOH), and protamex (POH) to evaluate their efficacy in mitigating dexamethasone-induced muscle damage in C2C12 cells in vitro. AOH exhibited notable cell proliferative abilities, promoting dose-dependent myotube formation. These results were further solidified by protein expression analysis. Western blot and gene expression analysis via RT-qPCR demonstrated that AOH downregulated MuRF-1, Atrogin, Smad 2/3, and Foxo-3a, while upregulating myogenin, MyoD, myosin heavy chain expression, and mTOR, key components of the ubiquitin-proteasome and mTOR signaling pathways. Finally, this study suggests that AOH holds promise for alleviating dexamethasone-induced muscle atrophy in C2C12 cells in vitro, offering insights for developing functional foods targeting conditions akin to sarcopenia.

Anti-obesity effects of red seaweed, Plocamium telfairiae, in C57BL/6 mice fed a high-fat diet.

This study aimed to demonstrate the anti-obesity effect of Plocamium telfairiae (PT), a red seaweed. Different percentages of ethanol (0%, 20%, 40%, 60%, 80%, and 100%) were used for the preparation of PT extract. Furthermore, 3T3-L1 cells were used to determine the percentage of ethanol for optimal anti-adipogenesis of PT, and the anti-obesity properties of the optimized extract of PT (PTE) (40%) was assessed in obese mice. The results indicate that 40% ethanol extract (40 PTE) significantly decreased fat accumulation and suppressed the expression of major adipogenesis factors such as peroxisome proliferator-activated receptor-γ (PPAR-γ), sterol regulatory element-binding protein 1 (SREBP-1), CCAAT/enhancer-binding protein (C/EBP)-α, and phosphorylated ACC (pACC) in 3T3-L1 cells. Furthermore, in the high-fat diet-induced obese mice, 40 PTE significantly reduced the weights of white adipose tissue, as well as the levels of triglyceride, total cholesterol, adiponectin, and insulin in the serum. Liver histopathology showed that steatosis decreased in all the PTE treatment groups. The adipogenesis-related proteins, PPAR-γ and SREBP-1, were also significantly decreased in PTE treatment groups. Additionally, 40 PTE increased mRNA expression of mitochondrial uncoupling proteins (UCP)-1 and UCP-3 in brown adipose tissue. These findings provide evidence that 40 PTE can alleviate lipid droplet accumulation in 3T3-L1 adipocytes and obese C57BL/6 mice, indicating that PTE has strong anti-obesity effects and could be used as a therapeutic agent or a component of pharmaceutical drugs and functional foods.

Anti-Obesity Effects of Grateloupia elliptica, a Red Seaweed, in Mice with High-Fat Diet-Induced Obesity via Suppression of Adipogenic Factors in White Adipose Tissue and Increased Thermogenic Factors in Brown Adipose Tissue.

Obesity is a serious metabolic syndrome characterized by high levels of cholesterol, lipids in the blood, and intracellular fat accumulation in adipose tissues. It is known that the suppression of adipogenic protein expression is an effective approach for the treatment of obesity, and regulates fatty acid storage and transportation in adipose tissues. The 60% ethanol extract of Grateloupia elliptica (GEE), a red seaweed from Jeju Island in Korea, was shown to exert anti-adipogenic activity in 3T3-L1 cells and in mice with high-fat diet (HFD)-induced obesity. GEE inhibited intracellular lipid accumulation in 3T3-L1 cells, and significantly reduced expression of adipogenic proteins. In vivo experiments indicated a significant reduction in body weight, as well as white adipose tissue (WAT) weight, including fatty liver, serum triglycerides, total cholesterol, and leptin contents. The expression of the adipogenic proteins, SREBP-1 and PPAR-γ, was significantly decreased by GEE, and the expression of the metabolic regulator protein was increased in WAT. The potential of GEE was shown in WAT, with the downregulation of PPAR-γ and C/EBP-α mRNA; in contrast, in brown adipose tissue (BAT), the thermogenic proteins were increased. Collectively, these research findings suggest the potential of GEE as an effective candidate for the treatment of obesity-related issues via functional foods or pharmaceutical agents.

Sargassum horneri (Turner) inhibit urban particulate matter-induced inflammation in MH-S lung macrophages via blocking TLRs mediated NF-κB and MAPK activation.

ETHNOPHARMACOLOGICAL RELEVANCE: Sargassum horneri is a nutrient rich edible brown seaweed with numerous biological properties found in shallow coastal areas of Korean peninsula. S. horneri traditionally used as a medicinal ingredient to treat several disease conditions such as hyperlipidemia, hypertension, heart disease, and inflammatory diseases (furuncle). However, to utilize S. horneri as an active ingredient for functional foods and human health applications requires to conform the bioactive properties and underlying mechanisms of those activities. AIM OF THE STUDY: Here, we investigated anti-inflammatory mechanisms of commercial grade 70% ethanol extract separated from S. horneri (SHE) on inflammatory response in particulate matter (PM)-induced MH-S lung macrophages; where PM in breathable air one of the major health concern in Korea. MATERIALS AND METHODS: We compared the anti-inflammatory effects of SHE on the activity of toll-like receptors (TLR) activation, NF-κB, MAPKs, and pro-inflammatory cytokine secretion in MH-S lung macrophages exposed to PM as a lung inflammation model. RESULTS: According to the results, PM-stimulation, induced the levels of NO, PGE2, TNF-α, IL-1ß, IL-6, iNOS, and COX2 (P < 0.05) in MH-S macrophages. In addition, phosphorylation levels of NF-κB and MAPKs were also increased with the PM stimulation through the upregulated expression of TLR. However, SHE treatment significantly repressed the secretions of inflammatory cytokines and reduced protein expression such as PGE2, TNF-α, IL-6, IL-1ß, NF-κB, and MAPKs from PM-activated macrophages. Specifically, SHE inhibited the upregulated mRNA expression levels of TLR2, TLR3, TLR4, and TLR7 in PM-induced MH-S cells; known biomarkers of downstream activation of NF-κB and MAPKs. CONCLUSION: These results suggested that SHE is a potential inhibitor of PM-induced inflammatory responses in lung macrophages. Thus, SHE could inhibit PM-induced chronic inflammation in lungs via blocking TLR/NF-κB/MAPKs signal transduction. Therefore, it was concluded that SHE may be a useful substance to develop as functional product to reduce inflammation against PM-induced inflammation.

The protective effect of Sargassum horneri against particulate matter-induced inflammation in lung tissues of an in vivo mouse asthma model.

Sargassum horneri is an edible brown seaweed with potential anti-inflammatory properties. The present study was designed to evaluate the anti-inflammatory properties of S. horneri using an in vivo mouse asthma model following exposure to particulate matter (PM). 7-8 week old BALB/c mice (20-25 g) were randomly divided into seven groups (n = 4) as follows: 1: no treatment, 2: OVA (ovalbumin) + PM, 3: OVA + PM + SHE (S. horneri ethanol extract) 200 mg kg-1, 4: OVA + PM + SHE 400 mg kg-1, 5: OVA + PM + prednisone 5 mg kg-1, 6: OVA only, and 7: PM only. All mice (except healthy controls) were sensitized on the first day by intraperitoneal injection of 10 µg OVA and 2 mg Al(OH)3 in 200 µL of saline. Starting from day 15, mice (except groups 1 and 6) were exposed to sonicated PM (5 mg m-3, 30 min day-1) through a nebulizer daily for 7 consecutive days. Mice exposed to PM and OVA showed up-regulated expression of MAPKs and pro-inflammatory cytokine production in the lungs. Furthermore, PM-exposed lungs had significantly reduced expression of Nrf2 and HO-1 genes. However, oral administration of the SHE reduced the phosphorylation levels of MAPKs, iNOS and COX2 expression levels, and mRNA expression levels of pro-inflammatory cytokines. In addition, SHE treated group mice had up-regulated anti-oxidant gene expression levels in the lungs compared to group 2. These findings demonstrate that oral administration of the SHE re-establishes PM-induced inflammation and oxidative stress in the lungs. Taken together, the SHE has therapeutic potential in preventing PM-induced inflammation and oxidative stress.