Hydroethanolic extract of Baccharis trimera promotes gastroprotection and healing of acute and chronic gastric ulcers induced by ethanol and acetic acid

Abstract

Ethanol is a psychoactive substance highly consumed around the world whose health problems include gastric lesions. Baccharis trimera is used in folk medicine for the treatment of gastrointestinal disorders. However, few studies have evaluated its biological and toxic effects. To validate the popular use of B. trimera and elucidate its possible antiulcerogenic and cytotoxic mechanisms, a hydroethanolic extract of B. trimera (HEBT) was evaluated in models of gastric lesions. Rats and mice were used to evaluate the protective and antiulcerogenic effects of HEBT on gastric lesions induced by ethanol, acetic acid, and chronic ethanol consumption. The effects of HEBT were also evaluated in a pylorus ligature model and on gastrointestinal motility. The LD50 of HEBT in mice was additionally estimated. HEBT was analyzed by nuclear magnetic resonance, and a high-performance liquid chromatography fingerprint analysis was performed. Oral HEBT administration significantly reduced the lesion area and the oxidative stress induced by acute and chronic ethanol consumption. However, HEBT did not protect against gastric wall mucus depletion and did not alter gastric secretory volume, pH, or total acidity in the pylorus ligature model. Histologically, HEBT accelerated the healing of chronic gastric ulcers in rats, reflected by contractions of the ulcer base. Flavonoids and caffeoylquinic acids were detected in HEBT, which likely contributed to the therapeutic efficacy of HEBT, preventing or reversing ethanol- and acetic acid-induced ulcers, respectively. HEBT antiulcerogenic activity may be partially attributable to the inhibition of free radical generation and subsequent prevention of lipid peroxidation. Our results indicate that HEBT has both gastroprotective and curative activity in animal models, with no toxicity.

Antioxidant, Gastroprotective, Cytotoxic Activities and UHPLC PDA-Q Orbitrap Mass Spectrometry Identification of Metabolites in Baccharis grisebachii Decoction

“…Moreover, the lyophilized extract of B. trimera showed a reduction of 90% of the lesion area at a dose of 400 mg/kg [29]. On the other hand, the cytoprotective effect of the hydroethanolic extract of this species was evaluated in two models of gastric lesions: induced by ethanol and acetic acid; which showed a significant reduction in the area of the lesion and oxidative stress induced by the consumption of necrotizing agents [30].…”

Antiulcer Agents: From Plant Extracts to Phytochemicals in Healing Promotion

“…The anti-secretory and antiulcer activity of B. trimera aqueous extract (1000–2000 mg/kg) was already reported in stress-induced ulcer model and pylorus ligature model [ 34 ] and even in a model of hydrochloric-induced acute gastric ulcers, where a lower dose (100–400 mg/kg) displayed antiulcer activity too [ 35 ]. In a more recent research performed, using a lower dose and a more concentrated B. trimera extract (90%), it was shown that the oral administration of 30 mg/kg significantly reduced the lesion area and the macroscopic appearance of acute and chronic ulcer models [ 36 ]. Also, in a study performed using high doses (1000–2000 mg/kg), the authors proposed that B. trimera inhibits gastric acid secretion by acting on the cholinergic regulatory pathway.…”

“…Also, in a study performed using high doses (1000–2000 mg/kg), the authors proposed that B. trimera inhibits gastric acid secretion by acting on the cholinergic regulatory pathway. However, Lívero et al [ 36 ] proposed that the effects of B. trimera extract in preventing or reversing ethanol- and acetic acid-induced ulcers may be attributable to the inhibition of free radical generation and subsequent prevention of lipid peroxidation and that flavonoids and caffeoylquinic acids detected in the studied extract play an important and contributive role on these effects.…”

Chrysin Modulates Genes Related to Inflammation, Tissue Remodeling, and Cell Proliferation in the Gastric Ulcer Healing

“…Alcoholism, besides smoking, stress, and H. pylori infection, is considered a risk factor for peptic ulcers. The chronic consumption of ethanol leads to gastric ulceration, reducing mucus production, cell proliferation, and gastric blood flow and promoting an inflammatory response [12]. Figure 1 shows the protective effect of chrysin in the model of gastric ulcer induced by absolute ethanol.…”