Background and Objectives: The plant Muscari Mill. is employed in both raw and cooked forms for the treatment of gastric diseases, as an expectorant, and for the treatment of warts and the enhancement of urine. A review of the scientific literature revealed no studies investigating the effect of Muscari neglectum (MN) water extract on gastric diseases. The objective of this study was to determine the effect of a water extract of the MN plant on indomethacin-induced gastric ulcer in rats, using a series of biochemical (SOD, CAT, GSH and MDA levels) and histopathological parameters. Methods: 60 male Sprague Dawley rats were utilized for the purposes of evaluating the acute toxicity and gastric ulcer models, with a total of 36 rats employed for these experiments (n = 6). The rats were divided into six groups: intact; indomethacin; famotidine; indomethacin and MN (100, 200, 400 mg/kg). Results: The Gastric tissue examinations at biochemical, macroscopic and pathological levels showed that MN extracts effectively prevented indo-methacin-induced gastric mucosal damage. The 400 mg/kg dose exhibited the most effective antiulcer effect, with a 69% protective efficacy. This dose caused an increase in the SOD, CAT and GSH levels and a decrease in the MDA levels compared to the IND group. Furthermore, an LC-MS/MS analysis was conducted on the water extract of MN, resulting in the identification of 14 phenolic compounds. Conclusions: Biochemical analyses and histopathological examinations demonstrated that the water extract of MN exhibited a beneficial protective effect against gastric ulceration due to its high antioxidant content.

Cadmium (Cd) is a toxic heavy metal and a significant environmental contaminant known to cause hepatotoxicity through mechanisms involving oxidative stress, inflammation, and apoptosis. Syringic acid (Sa), a naturally occurring phenolic compound, exhibits potent antioxidant and anti-inflammatory activities. This study aimed to evaluate the protective effects of SA against Cd-induced liver injury in rats. Fifty adult male Sprague-Dawley rats were randomly allocated into five groups (n= 10 per group): Control, Sa 100, Cd, Sa 50+Cd and Sa 100+Cd. Cadmium and/or SA were administered orally for 7 consecutive days. Biochemical markers of oxidative stress (SOD, GSH, CAT, and MDA), pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), and molecular indicators of inflammation (TLR-4, NF-κB) and apoptosis (Bax, Bcl-2, Caspase-3) were measured in liver tissue homogenates. Cadmium exposure significantly decreased the hepatic antioxidant enzyme activities (SOD, GSH, and CAT) and increased MDA and TLR-4 levels, indicating enhanced oxidative damage and inflammatory activation. Additionally, NF-κB, TNF-α, IL-1β, and IL-6 levels were markedly elevated following Cd administration. Apoptotic changes were evident by increased Bax and Caspase-3 expression and decreased Bcl-2 levels. Syringic acid co-administration dose-dependently ameliorated these pathological alterations, restoring oxidative balance, suppressing inflammation, and modulating apoptotic signaling. Syringic acid effectively attenuates cadmium-induced liver toxicity in rats by mitigating oxidative stress, suppressing pro-inflammatory responses, and regulating apoptosis-related pathways. These findings suggest that SA may serve as a promising hepatoprotective agent in conditions of heavy metal-induced hepatic injury.

Glyphosate (GLY) is a widely used herbicide active ingredient applied in agricultural, residential, and public areas. Although the European Chemicals Agency has stated that current evidence is insufficient to classify GLY as an endocrine disruptor, increasing experimental data indicate that GLY may induce organ toxicity. This study aimed to investigate glyphosate‐induced liver toxicity and to evaluate the potential protective effects of eugenol in a rat model. Eugenol is a phenolic compound predominantly found in clove oil (Syzygium aromaticum L.) and is known for its antioxidant, anti‐inflammatory, antimicrobial, and analgesic properties. It is classified as generally recognized as safe (GRAS) and non‐mutagenic by the World Health Organization. Thirty‐five male rats were randomly assigned to five groups: Control, EU‐100, GLY, GLY + EU‐50, and GLY + EU‐100. All treatments were administered orally by gavage. Oxidative stress markers (lipid peroxidation, reduced glutathione, and superoxide dismutase), liver enzyme activities (ALT, AST, and ALP), and the expression of genes involved in antioxidant defense, apoptosis, and inflammation (HO‐1, Nrf2, CAT, GPx, Bax, Caspase‐3, Bcl‐2, COX‐2, NF‐κB, IL‐6, TNF‐α, and IL‐1β) were analyzed. Short‐term GLY exposure resulted in oxidative imbalance, inflammatory activation, and apoptosis in hepatic tissue. Eugenol administration significantly alleviated these alterations by enhancing antioxidant defenses, activating the Nrf2/HO‐1 signaling pathway, and suppressing pro‐inflammatory responses. These findings suggest that eugenol may represent a promising natural hepatoprotective agent against glyphosate‐induced liver toxicity.