The objective of this study was to evaluate the pharmacological mechanisms involved in anti-inflammatory and antidiarrheal actions of hydroalcoholic extract obtained from the leaves of Cissus sicyoides (HECS). The anti-inflammatory effect was evaluated by oral administration of HECS against acute model of edema induced by xylene, and the mechanisms of action were analysed by involvement of arachidonic acid (AA) and prostaglandin E2 (PGE2). The antidiarrheal effect of HECS was observed and we analyzed the motility and accumulation of intestinal fluid. We also analyzed the antidiarrheal mechanisms of action of HECS by evaluating the role of the opioid receptor, α2 adrenergic receptor, muscarinic receptor, nitric oxide (NO) and PGE2. The oral administration of HECS inhibited the edema induced by xylene and AA and was also able to significantly decrease the levels of PGE2. The extract also exhibited significant anti-diarrheal activity by reducing motility and intestinal fluid accumulation. This extract significantly reduced intestinal transit stimulated by muscarinic agonist and intestinal secretion induced by PGE2. Our data demonstrate that the mechanism of action involved in the anti-inflammatory effect of HECS is related to PGE2. The antidiarrheal effect of this extract may be mediated by inhibition of contraction by acting on the intestinal smooth muscle and/or intestinal transit.

Peptic ulcer disease (PUD) is a multifactorial and complex disease caused by an imbalance of protective and aggressive factors (endogenous and exogenous). Despite advances in recent years, it is still responsible for substantial mortality and triggering clinical problems. Over the last decades, the understanding of PUD has changed a lot with the discovery of Helicobacter pylori infection. However, this disease continues to be a challenge due to side-effects, incidence of relapse from use of various anti-ulcer medicines, and the rapid appearance of antimicrobial resistance with current H. pylori therapies. Consequently, there is the need to identify more effective and safe anti-ulcer agents. The search for new therapies with natural products is a viable alternative and has been encouraged. The literature reports the importance of monoterpenes based on the extensive pharmacological action of this class, including wound healing and anti-ulcerogenic agents. In the present study, 20 monoterpenes with anti-ulcerogenic properties were evaluated by assessing recent in vitro and in vivo studies. Here, we review the anti-ulcer effects of monoterpenes against ulcerogenic factors such as ethanol, nonsteroidal anti-inflammatory drugs (NSAIDs), and Helicobacter pylori, highlighting challenges in the field.Biomolecules 2020, 10, 265 2 of 18 PUD results from an imbalance in mucosal defensive factors, such as mucus secretion, bicarbonate efflux, endogenous antioxidant, cell regeneration, continuous synthesis and release of prostaglandin E 2 (PGE 2 ), nitric oxide (NO), and sulfhydryl compounds (SH); and aggressive agents such as smoking, alcohol consumption, dietary factors, stress, prolonged and excessive intake of nonsteroidal anti-inflammatory drugs (NSAIDs), and Helicobacter pylori (H. pylori) infection, among others [6][7][8][9]. For a long time, it was believed that the main factor implicated in the development and progression of peptic ulceration was an hypersecretory acidic environment and together with dietary factors and/or stress was thought to cause most of PUD. But the discovery of H. pylori infection and the widespread use of NSAIDs in the second half of the 20 th century changed this perception. In recent years, peptic ulcer has been found to have multiple causes-H. pylori infection, NSAIDs, smoking, alcohol consumption, stress, lifestyle, and genetic predispositions are determined as major risk factors for the development of PUD [2]. PathophysiologyUnder normal conditions, gastric and duodenal mucosa integrity is maintained by the mucus-bicarbonate barrier, the neutral pH, and continuous epithelial cell renewal [10,11]. PGE 2 stimulates cell proliferation, mucus, and bicarbonate production, promoting a crucial function in mucosa preservation. Another vital factor in gastric homeostasis is adequate blood flow. The NO and PGs are responsible for the maintenance of proper perfusion to the gastric mucosa, assuring the delivery of oxygen and nutrients, as well as removing toxic metabolites, preventing damages to the ti...

Chrysin exhibits anti-inflammatory and antioxidant activities. Here, the gastroprotective effect of chrysin was investigated in mouse models of gastric ulcer induced by absolute ethanol, acetic acid, and ischemia-reperfusion injury. The gastric-healing effect was evaluated at 7 and 14 days after treatment; the mechanism of action was verified using the expression of metalloproteinase 2 (MMP-2) and 9 (MMP-9), caspase-3, cyclooxygenase 1 (COX-1) and 2 (COX-2), epidermal growth factor (EGF), and interleukin-10. Chrysin (10 mg/kg) inhibited macroscopic lesions and increased catalase activity in the mouse model established using absolute ethanol. It ameliorated the gastric ulcer caused by acetic acid by improving the expression of inflammatory genes such as COX-2, inhibiting negative remodeling promoted by MMP-9, increasing cell proliferation effect via EGF, and reducing cellular apoptosis by modulating caspase-3. A faster healing effect was evident in the first 7 days of treatment compared to 14 days of treatment, indicating the pharmacological potential of chrysin. Overall, these results demonstrate the potent effect of chrysin in the gastrointestinal tract and elucidate the genes involved in the healing of gastric ulcers. Moreover, an increase in the levels of gastric mucosa defensive factors is involved in the activity of chrysin in the gastric mucosa.

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The project encompasses plants from the following families: Palmae, Lamiaceae, Acanthaceae, Leguminosae and Gesneriaceae. Regarding the pharmacology, several models have been used like antinociceptive, antiinflammatory, antioxidant, molluscicidal, anti-diabetes, anti-microbial and nitric oxide production inhibition. Results showed that utilizing ethnopharmacological information is a very important way to search for new bioactive molecules. It is noteworthy to mention the activity of Açaí fruit extracts in the inhibition of nitric oxide production. It was also possible to identify flavonoids responsible for the antidiabetic activity in plants belonging to the family Leguminosae. Acanthaceae extracts showed important antinociceptive and anti-inflammatory activities, as they are very rich in steroids and triterpenes. The same could be said about plants belonging to Lamiaceae that gave several examples of this kind of pharmacological property due to its steroid and triterpenoid compounds. One specie of Lamiaceae also produced a great amount of dihydroxylated triterpenoids with great molluscicidal potencial. Palmae species, rich in fatty acids and steroids led to enriched extracts responsible for the anti-BPH activities. Plants belonging to Gesneriaceae were antioxidant due to their flavonoid content. Polar extracts and isolated molecules, isolated from many species were able to donate hydrogen radical to DPPH.

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Citral is a mixture of monoterpenes present in the essential oil of several plants, such as Cymbopogon citratus and Zingiber officinale, possessing anti-inflammatory, anti-ulcerogenic, and antipyretic actions. We investigated the action of citral on body temperature (Tb) and inflammatory signaling in eutrophic and obese mice during Systemic Inflammation (SI) induced by Lipopolysaccharide (LPS). Thus, we assessed the effect of citral (25, 100, and 300 mg/kg) and ibuprofen in LPS-induced SI in Swiss male mice fed a standard diet (SD) or high-fat diet (HFD) for 12 weeks. Following SI induction, we measured Tb and collected the serum, hypothalamus, and gastric mucosa for biochemical measurements. Acute treatment with citral decreased the Tb of both SD and HFD-fed animals. Citral (300 mg/kg) treatment caused a significantly lower Tb variation in HFD-fed animals than in those fed the SD. Citral reduced peripheral levels of tumor necrosis factor (TNF)-α in SD and HFD mice and decreased serum leptin concentration in HFD mice 90 min after the LPS challenge. Furthermore, citral also reduced interleukin (IL)-6 levels in the hypothalamus of obese mice. In summary, citral effectively reduced Tb during SI by reducing inflammatory mediators with a distinct action profile in HFD mice when compared with SD.