Gastroprotective effect of limonene in rats: Influence on oxidative stress, inflammation and gene expression

Souza, Matheus Chiaradia de; Vieira, Ana Júlia; Beserra, Fernando Pereira; Pellizzon, Cláudia Helena; Nóbrega, Rafael Henrique; Rozza, Ariane Leite

doi:10.1016/j.phymed.2018.09.027

Cited by 118 publications

(67 citation statements)

References 30 publications

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“…In addition, some previous studies reported that the extract of A. officinarum has anti-inflammatory activity (Jeong et al 2008;Elgazar et al 2018;Gong et al 2018), which provides us with the theoretical basis of F-AOH treatment against gastric ulcer. Ethanol stimulation is associated with a sharp increase in the levels of proinflammatory factors in gastric tissue, congestion and oedema of gastric mucosa (Boutemine et al 2018), death of epithelial cells, local or multiple haemorrhagic ulcers (Tarnawski et al 1987), and tissue degeneration and necrosis (de Souza et al 2019). These changes are consistent with our experimental results, and the pre-treatment of F-AOH significantly reduces these changes.…”

Section: Discussionsupporting

confidence: 90%

Protective effects of total flavonoids from Alpinia officinarum rhizoma against ethanol-induced gastric ulcer in vivo and in vitro

Wang

Gong

et al. 2020

Pharmaceutical Biology

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Context: Alpinia officinarum Hance (Zingiberaceae) is traditionally used to treat inflammation, pain, colds and digestive diseases. Objective: To investigate the potential protective mechanism of total flavonoids from the rhizomes of A. officinarum (F-AOH) in ethanol-induced acute gastric in vivo and in vitro. Materials and methods: In vivo: Gastric damage was induced in BALB/c mice by administering ethanol (10 mL/kg) after oral treatment with F-AOH at 126.8, 63.4 and 31.7 mg/kg or ranitidine (Ran) at 100 mg/kg (1 week of continuous gavage). In vitro: Gastric mucosal epithelial cells (GES-1) were incubated with F-AOH (8, 4 and 2 lg/mL) for 16 h and treated with 7% ethanol for 4 h. The extent of gastric damage was assessed histopathologically, and the expression of NF-jB, COX-2, TNF-a, iNOS and IL-1b was quantified by Western blot analysis. In addition, proinflammatory mediators and concentrations of motilin (MTL) and gastrin (GAS) were measured by ELISA test. Results: F-AOH effectively reduced the ulcer index (from 23.4 ± 4.28 to 8.32 ± 1.5) and reduced release of inflammatory mediators (IL-1b, IL-6, TNF-a and PGE2), increased the content of nitric oxide and improved GAS and MTL secretion. The 50% inhibitory concentration (IC 50) of F-AOH on cell damage was 17 lg/mL. F-AOH increased ethanol-induced cell survival (from 47 to 85%) and inhibited the expression of NF-jB, COX-2, TNF-a, IL-1b and iNOS proteins. Conclusions: F-AOH inhibits ethanol-induced gastric mucosal damage, provides a theoretical basis for galangal in the treatment of other causes of GU, and promotes the application of galanga in the treatment of GU.

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Section: Discussionsupporting

confidence: 90%

Protective effects of total flavonoids from Alpinia officinarum rhizoma against ethanol-induced gastric ulcer in vivo and in vitro

Wang

Gong

et al. 2020

Pharmaceutical Biology

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“…For instance, the same group described a gastric protection effect in rats with colon inflammation [103], and in an animal model of an ulcer induced by ethanol and indomethacin [106]. In addition, D-limonene-induced mucus production and IL-6, IL-1β, and TNF inhibition has been previously described [107]. Corroborating this data, Wang and colleagues demonstrated that limonene affected the intestinal microbiota of mice and enhanced the relative abundance of Lactobacillus, suggesting limonene direct effects on intestinal bacteria [108].…”

Section: D-limonenementioning

confidence: 94%

Terpenoids, Cannabimimetic Ligands, beyond the Cannabis Plant

et al. 2020

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Medicinal use of Cannabis sativa L. has an extensive history and it was essential in the discovery of phytocannabinoids, including the Cannabis major psychoactive compound—Δ9-tetrahydrocannabinol (Δ9-THC)—as well as the G-protein-coupled cannabinoid receptors (CBR), named cannabinoid receptor type-1 (CB1R) and cannabinoid receptor type-2 (CB2R), both part of the now known endocannabinoid system (ECS). Cannabinoids is a vast term that defines several compounds that have been characterized in three categories: (i) endogenous, (ii) synthetic, and (iii) phytocannabinoids, and are able to modulate the CBR and ECS. Particularly, phytocannabinoids are natural terpenoids or phenolic compounds derived from Cannabis sativa. However, these terpenoids and phenolic compounds can also be derived from other plants (non-cannabinoids) and still induce cannabinoid-like properties. Cannabimimetic ligands, beyond the Cannabis plant, can act as CBR agonists or antagonists, or ECS enzyme inhibitors, besides being able of playing a role in immune-mediated inflammatory and infectious diseases, neuroinflammatory, neurological, and neurodegenerative diseases, as well as in cancer, and autoimmunity by itself. In this review, we summarize and critically highlight past, present, and future progress on the understanding of the role of cannabinoid-like molecules, mainly terpenes, as prospective therapeutics for different pathological conditions.

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“…In experimental models involving the administration of absolute ethanol, ethanol 70%, or ethanol plus HCl (in different proportions), pretreatment with monoterpenes significantly reduced lesion areas and increased the production of mucus, SH, NO, and PGs, exhibiting an important gastroprotective effect. In animal models, carvacrol [63], citronellol [64], geraniol [67], epoxy-carvone [52], α-pinene [60], myrtenol [58], α-terpineol [61], linalyl acetate [55], menthol [56,57], nerol [59], eucalyptol [51], limonene [43,44], thymol [70], and β-myrcene [67] reduced up to 100% of the gastric lesions caused by ethanol administration (Table 1). In this review, we observed that the isomers of two bicyclic monoterpenes presented different anti-ulcer effects.…”

Section: Ethanolmentioning

confidence: 99%

“…Therefore, cytokines such as TNF-α, IL-6, and IL-10 are important factors in the severity of gastric ulcers [100]. The monoterpene limonene displayed anti-inflammatory activity by decreasing TNF-α, IL-6, and IL-1β and increasing the level of IL-10 [44,62,63].…”

Section: Mechanisms Of Action Of the Peptic Ulcersmentioning

confidence: 99%

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Systematic Analysis of Monoterpenes: Advances and Challenges in the Treatment of Peptic Ulcer Diseases

et al. 2020

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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...

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Gastroprotective effect of limonene in rats: Influence on oxidative stress, inflammation and gene expression

Cited by 118 publications

References 30 publications

Protective effects of total flavonoids from Alpinia officinarum rhizoma against ethanol-induced gastric ulcer in vivo and in vitro

Protective effects of total flavonoids from Alpinia officinarum rhizoma against ethanol-induced gastric ulcer in vivo and in vitro

Terpenoids, Cannabimimetic Ligands, beyond the Cannabis Plant

Systematic Analysis of Monoterpenes: Advances and Challenges in the Treatment of Peptic Ulcer Diseases

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