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1.
Oncol Lett ; 27(6): 245, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38638846

ABSTRACT

[This corrects the article DOI: 10.3892/ol.2018.8364.].

2.
Neuro Endocrinol Lett ; 42(8): 528-537, 2021 Dec 21.
Article in English | MEDLINE | ID: mdl-35490418

ABSTRACT

BACKGROUND AND AIMS: An ulcerative colitis rat model was established with baicalin as the treatment. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction (QRT-PCR) and Western blot analysis were used to determine inflammatory factor expression in interstitial cells of Cajal. RESULTS: Baicalin treatment reduced the ulcerative colitis symptoms, such as bloody diarrhea, reduction in body weight, and vomiting. Baicalin treatment decreased the serum levels of tumor necrosis factor α (TNFα), interleukin (IL)-1ß, and IL-17A compared to the phosphate buffer saline (PBS) control group. Baicalin treatment protected the interstitial cells of Cajal against oxidative stress injury via improvements in superoxide dismutase (SOD) activity, modified disease activity index (mDAI), reactive oxygen species (ROS) production, catalase (CAT), glutathione (GSH), and nitric oxide (NO) level in the serum and interstitial cells of Cajal. Baicalin treatment decreased apoptosis of interstitial cells of Cajal. Baicalin treatment decreased the nuclear factor Kappa B (NF-κB)/ Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/ extracellular regulated kinase (Erk) / protein kinase B (Akt) signal pathway in interstitial cells of Cajal and NF-κB overexpression abrogated the decreased baicalin-induced inflammation and apoptosis of interstitial cells of Cajal induced. CONCLUSION: Baicalin treatment improved ulcerative colitis symptoms and decreased inflammation and apoptosis of interstitial cells of Cajal. Baicalin treatment inhibited inflammation and apoptosis of interstitial cells of Cajal by targeting the NF-κB pathway in an ulcerative colitis rat model, which may serve as a potential agent for the treatment of ulcerative colitis.

3.
Oncol Lett ; 15(6): 8744-8748, 2018 Jun.
Article in English | MEDLINE | ID: mdl-29805612

ABSTRACT

Colorectal cancer is cancer of the colon or rectum and is the third most prevalent form of cancer. Currently, there are several shortcomings in the prognosis and early detection of colon cancer. The present study aims to address questions pertaining to the role of microRNA (miR)-137 in colon cancer progression and the mode of regulation. The endogenous and over-expressed levels of miR-137 in three colon cancer cell lines were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The MTT assay was used to assess cell proliferation. Cell migration and invasion assays were assessed using Transwell apparatus and Matrigel invasion chambers. The potential targets of miR-150 were predicted using TargetScan software, and one of the best scoring targets, transcription factor 4 (TCF4), was experimentally validated using western blot analysis and RT-qPCR. It was found that that miR-137 is expressed at extremely low levels in COLO205, HCT116 and SW480 cell lines. Cell proliferation, migration and invasion were inhibited subsequent to transfection of the colon cancer cell lines with miR-137. Using bioinformatics analysis, the best scoring putative targets were identified. One such target, TCF4, was experimentally validated, and it was shown that overexpression of miR-137 suppresses TCF4 in all three colon cancer cell lines. In conclusion, it was shown that miR-137 inhibits cell proliferation, migration and invasion in colon cancer cell lines by negatively regulating the expression of TCF4.

4.
Med Sci Monit ; 23: 1146-1155, 2017 Mar 05.
Article in English | MEDLINE | ID: mdl-28259893

ABSTRACT

BACKGROUND Colorectal adenocarcinoma is the second leading cause of cancer-related death in the world. The stage of the disease is related to the survival of the patient, and in early phases surgery is the main modality of treatment. The main aim of modern medicinal chemistry is to synthesize small molecules via drug designing, especially by targeting tumor cells. MATERIAL AND METHODS A new series of 19 compounds containing benzothiazole and thiazole were designed. Molecular docking studies were performed on the designed series of molecules. Compounds showing good binding affinity towards the EGFR receptor were selected for synthetic studies. Characterization of the synthesized compounds was done by FTIR, 1HNMR, Mass and C, H, N, analysis. RESULTS The anticancer evaluation of the synthesized compounds was done at NIC, USA at a single dose against colon cancer cell lines HCT 116, HCT15, and HC 29. The active compounds were further evaluated for the 5-dose testing. Compounds were designed by using docking analysis. To ascertain the interaction of EGFR tyrosine kinase binding, energy calculation was used. CONCLUSIONS The results of the present study indicate that the designed compounds show good activity against colon cancer cell lines, which may be further studied to design new potential molecules.


Subject(s)
Colonic Neoplasms/pathology , Drug Design , Drug Screening Assays, Antitumor , Adenosine Triphosphate , Antineoplastic Agents/chemistry , Antineoplastic Agents/pharmacology , Benzothiazoles/chemistry , Benzothiazoles/pharmacology , Binding Sites , Cell Line, Tumor , Cell Proliferation/drug effects , Crystallography, X-Ray , Dose-Response Relationship, Drug , Humans , Hydrogen Bonding , Hydrophobic and Hydrophilic Interactions , Molecular Docking Simulation
5.
World J Gastroenterol ; 20(45): 17020-8, 2014 Dec 07.
Article in English | MEDLINE | ID: mdl-25493014

ABSTRACT

Gastric ulcer is a common disorder of the digestive system. Current therapeutic regimens largely rely on Western medicine. However, numerous studies have demonstrated that herbal medicines can effectively treat gastric ulcer in humans and various animal models via divergent mechanisms. This review updates the efficacy and safety of herbal medicines in treating gastric ulcer, and the mechanisms of their action in humans and animal models. Studies have demonstrated that the efficacy of herbal medicines is comparable or superior to that of drugs such as omeprazole or cimetidine in humans and animal models, and herbal medicines display fewer adverse effects. The mechanisms by which herbal medicines benefit gastric ulcer include stimulation of mucous cell proliferation, anti-oxidation, and inhibition of gastric acid secretion and H(+)/K(+)-ATPase activity. Some herbal medicines also exhibit antimicrobial properties. Utilization of herbal medicines could be a valuable alternative to treat gastric ulcer in humans effectively, with few adverse effects.


Subject(s)
Anti-Ulcer Agents/therapeutic use , Gastric Mucosa/drug effects , Plant Preparations/therapeutic use , Stomach Ulcer/drug therapy , Animals , Anti-Ulcer Agents/adverse effects , Antioxidants/therapeutic use , Gastric Acid/metabolism , Gastric Mucosa/metabolism , Gastric Mucosa/pathology , Humans , Phytotherapy , Plant Preparations/adverse effects , Plants, Medicinal , Proton Pump Inhibitors/therapeutic use , Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors , Sodium-Potassium-Exchanging ATPase/metabolism , Stomach Ulcer/metabolism , Stomach Ulcer/pathology , Treatment Outcome , Wound Healing/drug effects
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