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Helicobacter pylori (H. pylori) causes gastric mucosa inflammation and gastric cancer mostly via several virulence factors. Induction of proinflammatory pathways plays a crucial role in chronic inflammation, gastric carcinoma, and H. pylori pathogenesis. Herbal medicines (HMs) are nontoxic, inexpensive, and mostly anti‐inflammatory reminding meticulous emphasis on the elimination of H. pylori and gastric cancer. Several HM has exerted paramount anti‐H. pylori traits. In addition, they exert anti‐inflammatory effects through several cellular circuits such as inhibition of 5′‐adenosine monophosphate‐activated protein kinase, nuclear factor‐κB, and activator protein‐1 pathway activation leading to the inhibition of proinflammatory cytokines (interleukin 1α [IL‐1α], IL‐1β, IL‐6, IL‐8, IL‐12, interferon γ, and tumor necrosis factor‐α) expression. Furthermore, they inhibit nitrous oxide release and COX‐2 and iNOS activity. The apoptosis induction in Th1 and Th17‐polarized lymphocytes and M2‐macrophagic polarization and STAT6 activation has also been exhibited. Thus, their exact consumable amount has not been revealed, and clinical trials are needed to achieve optimal concentration and their pharmacokinetics. In the aspect of bioavailability, solubility, absorption, and metabolism of herbal compounds, nanocarriers such as poly lactideco‐glycolide‐based loading and related formulations are helpful. Noticeably, combined therapies accompanied by probiotics can also be examined for better clearance of gastric mucosa. In addition, downregulation of inflammatory microRNAs (miRNAs) by HMs and upregulation of those anti‐inflammatory miRNAs is proposed to protect the gastric mucosa. Thus there is anticipation that in near future HM‐based formulations and proper delivery systems are possibly applicable against gastric cancer or other ailments because of H. pylori.
Helicobacter pylori (H. pylori) causes gastric mucosa inflammation and gastric cancer mostly via several virulence factors. Induction of proinflammatory pathways plays a crucial role in chronic inflammation, gastric carcinoma, and H. pylori pathogenesis. Herbal medicines (HMs) are nontoxic, inexpensive, and mostly anti‐inflammatory reminding meticulous emphasis on the elimination of H. pylori and gastric cancer. Several HM has exerted paramount anti‐H. pylori traits. In addition, they exert anti‐inflammatory effects through several cellular circuits such as inhibition of 5′‐adenosine monophosphate‐activated protein kinase, nuclear factor‐κB, and activator protein‐1 pathway activation leading to the inhibition of proinflammatory cytokines (interleukin 1α [IL‐1α], IL‐1β, IL‐6, IL‐8, IL‐12, interferon γ, and tumor necrosis factor‐α) expression. Furthermore, they inhibit nitrous oxide release and COX‐2 and iNOS activity. The apoptosis induction in Th1 and Th17‐polarized lymphocytes and M2‐macrophagic polarization and STAT6 activation has also been exhibited. Thus, their exact consumable amount has not been revealed, and clinical trials are needed to achieve optimal concentration and their pharmacokinetics. In the aspect of bioavailability, solubility, absorption, and metabolism of herbal compounds, nanocarriers such as poly lactideco‐glycolide‐based loading and related formulations are helpful. Noticeably, combined therapies accompanied by probiotics can also be examined for better clearance of gastric mucosa. In addition, downregulation of inflammatory microRNAs (miRNAs) by HMs and upregulation of those anti‐inflammatory miRNAs is proposed to protect the gastric mucosa. Thus there is anticipation that in near future HM‐based formulations and proper delivery systems are possibly applicable against gastric cancer or other ailments because of H. pylori.
The review classifies these ecofriendly synthesized Ru nanomaterials designed to date on the basis of their synthetic strategy.
Background:: Alteration in the expression and activity of drug-metabolizing enzymes (DMEs) can alter the pharmacokinetics and hence the response of the drug. Some chemicals found in herbs and fruits affect the expression of DMEs. Calamintha incana is commonly used in Middle Eastern Arabic countries. There is no report regarding the influence of Calamintha incana on the hepatic expression of DMEs. Aims:: The current investigation aimed to investigate the effect of Calamintha incana consump-tion on the mRNA expression of major hepatic drug-metabolizing cytochrome (cyp) P450 genes in mice. Methods:: The chemical composition of the ethanoic extract was analyzed using liquid chroma-tography/mass spectrometry. Then, 21 BALB/c mice were used for the in vivo experiment. The mice were divided into three groups, each consisting of seven mice. The first group (low-dose group) was treated with 41.6 mg/kg of Calamintha incana extract and the second group was administered the high-dose (125 mg/kg) of the extract for one month. The mice in the third “con-trol” group administrated the vehicle 20% polyethylene glycol 200. Then, the expression of cyp3a11, cyp2c29, cyp2d9, and cyp1a1 was analyzed using the real-time polymerase chain reac-tion. The relative liver weights of the mice and the hepatic pathohistological alterations were assessed. Results:: The ethanolic extract of Calamintha incana contained 27 phytochemical compounds. The most abundant compounds were linolenic acid, myristic acid, and p-cymene. It was found that the low dose of Calamintha incana extract upregulated significantly (P < 0.05) the expres-sion of cyp3a11 by more than ten folds in the liver of treated mice. Furthermore, the histological analysis showed that low- and high-dose administration of the C. incana did not cause patholog-ical alterations. Conclusion:: It can be concluded from these findings that consumption of low doses of Cala-mintha incana upregulated the mRNA expression of mouse cyp3a11 without causing histopatho-logical alterations in the livers. Further studies are needed to determine the influence of Cala-mintha incana on the pharmacokinetics and response of drugs metabolized by cyp3a11.
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