Methods: The mixture of IB and DJ extracts was analyzed for its total flavonoid content (TFC), total polyphenol content (TPC), and radical scavenging activities. Gastric lesions were induced by treating rats with 1 mL of a solution containing 60% ethanol and 150 mM HCl.The rats were then divided into 5 groups: CON (normal control), HEC (treated with 150 mM HCl-60% ethanol and distilled water), IBE (treated with 150 mM HCl-60% ethanol and IB extract at 350 mg/kg body weight [BW]), ID30 (treated with 150 mM HCl-60% ethanol and a mixture of IB and DJ extracts in a 7:3 ratio at 350 mg/kg BW), and DJE (treated with 150 mM HCl-60% ethanol and DJ extract at 350 mg/kg BW). Results: The ID30 group exhibited significantly higher TFC, TPC, and radical scavenging activities than the groups treated with single extracts. This group also showed a notable decrease in the formation of gastric lesions and preservation of gastric wall mucus. In addition, the serum levels of the inflammatory marker tumor necrosis factor (TNF)-α were significantly lower in the ID30 group than in the HEC group. Conclusion The antioxidants present in the ID30 mixture effectively reduced oxidative stress and reactive oxygen species, mitigating gastric mucosal irritation induced by alcohol and acid. Furthermore, the mixture inhibited gastric acid secretion and inflammatory marker expression, such as TNF-α, preventing tissue damage. These findings suggest that the ID30 mixture is a potential preventative treatment for gastritis.

Hyperammonemia is mainly caused by diseases related to liver failure. However, there are also non-hepatic causes of hyperammonemia, such as urinary tract infection (UTI) due to urease-producing organisms. Urease production by these bacteria induces a hydrolysis of urinary urea into ammonia that can cross the urothelial cell membrane and diffuse into blood vessels, leading to hyperammonemia. Delayed diagnosis and treatment of hyperammonemia can lead to lethal encephalopathy that can cause brain damage and life-threatening conditions. In the presence of obstructive uropathy, UTI by urease-producing bacteria can lead to more severe hyperammonemia due to enhanced resorption of ammonia into the systemic circulation. In this report, we present a case of acute severe hyperammonemic encephalopathy leading to brain death due to accumulation of ammonia in blood caused by Morganella morganii UTI in a 10-year-old girl with cloacal anomaly, causing obstructive uropathy even after multiple corrections.