Anxiety disorders are closely associated with oxidative stress-mediated neuronal damage, mitochondrial dysfunction, and apoptosis. In this study, we investigated the neuroprotective effects of Lactiplantibacillus plantarum HY7715 in a mouse model of restraint stress-induced anxiety, and in neuronal cell models (HT-22 mouse hippocampal neuroblast cell and SH-SY5Y human neuroblastoma cells). Oral administration of HY7715 (1 × 10⁹ CFU/kg/day) alleviated anxiety-like behaviors significantly, as shown by increased central exploration in the open field test and prolonged open-arm activity in the elevated plus maze. HY7715 reduced serum norepinephrine levels elevated by stress, and restored hippocampal expression of brain-derived neurotrophic factor, while suppressing pro-inflammatory (NF-κB, IL-6) and pro-apoptotic (BAX, caspase-3) markers. It also increased expression of mitochondrial regulatory genes (SIRT1, mTOR), and decreased that of cytochrome c, in brain tissue. Histological analysis revealed that HY7715 preserved neuronal integrity in the CA1 and CA3 hippocampal regions. In vitro, HY7715 attenuated oxidative stress-induced cytotoxicity, decreased intracellular ROS accumulation, maintained mitochondrial activity, and inhibited apoptosis of both neuronal cell types, showing greater efficacy than the strain type L. plantarum KCTC3108. These findings suggest that HY7715 exerts neuroprotective effects by modulating oxidative stress/apoptosis/mitochondrial pathways, and highlight its potential as a psychobiotic for stress-related neuropsychiatric disorders.

Chronic kidney disease (CKD) causes a variety of health problems including renal dysfunction and cardiovascular disease. This study aimed to investigate whether the probiotic strain Lactiplantibacillus plantarum HY7718 (HY7718) can protect against CKD using HK2 cells and a CKD mouse model, generated by feeding mice a diet containing 0.15% adenine. In vitro tests showed that HY7718 was anti-inflammatory in H₂O₂-treated HK2 cells and reduced apoptosis of tumor necrosis factor-α/cycloheximide-induced HK2 cells. In the adenine-induced CKD model, markers of renal dysfunction (blood urea nitrogen (BUN) and creatinine (Crea)) and inorganic calcium and phosphorus were markedly increased. However, oral administration of HY7718 (10⁸ colony-forming units/kg/day) significantly attenuated these increases. HY7718 also reduced the kidney histopathological score, including tubular necrosis, cast formation, and tubular dilatation, as well as the mononuclear cell infiltration score in kidney tissue, suggesting that it could reverse the progression of CKD. Additionally, HY7718 downregulated the renal expression of pro-inflammatory cytokine genes and members of the TLR/NF-κB signaling pathway. Furthermore, HY7718 reduced tubule apoptotic cells and expression of apoptosis-related genes, indicating that it is potentially renoprotective. These results demonstrate that supplementation with the probiotic HY7718 can ameliorate CKD symptoms by improving renal function and reducing kidney injury.

Alcohol-associated liver disease (ALD) contributes substantially to the global burden of chronic liver disease, yet few effective pharmacological treatments are currently available. The hepatoprotective potential of Lactobacillus helveticus HY7804 was evaluated in ethanol-exposed HepG2 cells and in a modified chronic-binge ethanol-fed mouse model adapted from the National Institute on Alcohol Abuse and Alcoholism (NIAAA) paradigm. Ethanol-induced cytotoxicity in HepG2 cells was attenuated by HY7804, as demonstrated by the recovery of cell viability and the reduction in lactate dehydrogenase release. HY7804 also decreased ethanol-induced inflammatory cytokine production, including IL-6, TNF-α, IL-1β, and IL-8, and modulated apoptosis-related gene expression. In chronic-binge ethanol-fed mice, HY7804 reduced serum AST from 183.4 ± 34.1 to 129.4 ± 16.4 U/L (p < 0.01) and ALT from 67.5 ± 4.5 to 52.1 ± 4.7 U/L (p < 0.05). Hepatic lipid accumulation was also significantly reduced by HY7804 treatment compared with the EtOH group, as indicated by the decreased Oil Red O-positive area (p < 0.01). Hepatic MDA levels decreased from 46.01 ± 3.38 to 30.58 ± 6.38 nmol/mg tissue (p < 0.01). In addition, HY7804 modulated hepatic inflammatory cytokine profiles, antioxidant-related responses, and the Bax/Bcl-2 expression ratio. These findings suggest that HY7804 mitigates ethanol-induced hepatic injury, with associated changes in inflammatory responses, antioxidant-related markers, lipid peroxidation, and apoptosis-related gene expression.