Muscle atrophy, a physiological decline in muscle mass and strength due in ageing, occurs through an imbalance between protein breakdown and synthesis. The purpose of this study was to verify whether amino acid complex supplementation (ACS) can prevent and treat muscle loss in a dexamethasone (Dexa, 800 μg/kg)-induced rat model of sarcopenia. Sprague Dawley rats (6 weeks old) were assigned to seven groups: (i) normal control, (ii) positive control (high-dose ACS, 500 mg), (iii) Dexa only, (iv) Dexa + high-dose ACS (500 mg), (v) Dexa + medium-dose ACS (300 mg), (vi) Dexa + low-dose ACS (100 mg), or (vii) Dexa + liquid amino acid complex formulation (LF, 2 mL), administered orally for 4 weeks. Exercise capacity tests were performed five times using a treadmill test (TT) and forced swimming test (FST). The body weight increase in each group was less than that of the normal group. The blood biochemical indices, AST levels, and AST/ALT ratio significantly increased in the Dexa-treated medium-dose ACS group. The total muscle protein also significantly increased in all ACS groups. In the Dexa-treated LF group, CK decreased below the normal level. Exercise capacity, assessed by TT and FST, increased the most in the positive control and Dexa-treated high-dose ACS groups. In the TT, the Dexa-only group increased by about 18%, but the Dexa-treated high-dose ACS group increased by about 110%. Additionally, in the FST, Dexa-treated rats receiving a high dose of ACS demonstrated significantly increased exercise time and capacity. Electron microscopic (EM) and hematoxylin and eosin (H&E) observations of muscle tissue revealed muscle fiber atrophy in the gastrocnemius muscles of the Dexa-only group. In the EM findings of the Dexa-treated high-dose ACS group, the M-line and Z-line were clearer than in the Dexa-only group, and the mitochondria were partially preserved. In conclusion, the ACS-treated rats showed a clear recovery from muscle damage based on serum indices, total muscle protein mass, and the microscopic findings on muscle tissue. Notably, a high dose of ACS demonstrated the most effective protection and recovery of muscle tissue in the Dexa-induced sarcopenia rat model.

Background/Objectives: Acetaminophen (APAP) is a widely used analgesic and antipyretic, but overdose can lead to APAP-induced liver injury (AILI), a major cause of acute liver failure. While N-acetylcysteine (NAC) is the current standard of care, its efficacy is significantly reduced when administered after the peak time of liver injury, highlighting the need for alternative therapeutic strategies. Human placenta hydrolysate (HPH) has shown potential as a therapeutic agent for various liver diseases due to its rich content of bioactive compounds. This study aimed to investigate the hepatoprotective effects of HPH in a mouse model of AILI. Methods: HPH was administered to mice for three days prior to APAP treatment. The effects of HPH on liver morphology, necrosis, liver enzymes, phase I/II detoxification enzymes, oxidative stress markers, and inflammatory cytokines were evaluated. Results: HPH pretreatment attenuated APAP-induced liver necrosis and congestion, reduced serum levels of liver enzymes. In addition, HPH showed a concentration-dependent attenuation of APAP-induced decrease in human hepatocyte viability. HPH modulated phase I/II enzyme expression by downregulating CYP2E1 and upregulating SULT1A1, UGT1A6, GSTP1, and TPMT. HPH also exhibited antioxidant effects by increasing SOD and GPx activities, reducing MDA levels, and restoring the GSH/GSSG ratio. Furthermore, HPH attenuated the APAP-induced increase in the inflammatory cytokines TNF-α and IL-6. These findings suggest that HPH protects against AILI through multiple mechanisms, including the modulation of phase I/II detoxification, activation of antioxidants, and inhibition of inflammation. Conclusions: HPH could be a potential therapeutic option for APAP overdose and related liver injuries.

Background: Alcoholic liver disease (ALD) represents a major global health burden, encompassing a spectrum of hepatic abnormalities ranging from steatosis to cirrhosis and hepatocellular carcinoma. Laennec, a human placenta-derived hydrolysate, was evaluated for its therapeutic effects on alcohol-induced fatty liver in an experimental animal model. Methods: Animals were pretreated with alcohol for 2 weeks, followed by the co-administration of alcohol and Laennec for 4 weeks. The study included four groups: normal control, alcohol-only, and low- and high-dose Laennec-treated groups. Results: Alcohol administration significantly elevated the serum ALT levels (3.17-fold vs. control), indicating hepatocellular injury, whereas Laennec treatment reduced the ALT levels in a dose-dependent manner. The AST levels increased in the alcohol-only group, although the change was not statistically significant; however, the AST levels decreased in the low-dose Laennec-treated groups. The AST/ALT ratio showed significantly dose-dependent recovery in the high-dose group. Laennec treatment attenuated hepatic lipid accumulation and inflammation, with the most pronounced effects observed in the high-dose group. Regarding alcohol-metabolizing enzymes, Laennec exhibited an inhibitory effect on alcohol-induced ADH activity, with no significant effect on ALDH. CYP2E1 activity was suppressed in a dose-dependent manner following Laennec administration. No significant changes were observed in the GPx activity. Additionally, high-dose Laennec significantly restored the catalase and STAT3 (Ser727) phosphorylation levels. Histopathological analysis (H&E staining) demonstrated marked reductions in lipid droplet accumulation and inflammatory cell infiltration in Laennec-treated groups compared to the alcohol-only group. Conclusion: These findings suggest that Laennec exerts hepatoprotective effects against alcohol-induced liver injury and steatosis, as evidenced by improvements in biochemical markers, enzyme activity, and histological features.