Sterol regulator element binding proteins (SREBPs) are a family of transcription factors involved in the biogenesis of cholesterol, fatty acids and triglycerides. They also regulate physiological functions of many organs, such as thyroid, brain, heart, pancreas and hormone synthesis. Beside the physiological effects, SREBPs participate in some pathological processes, diabetes, endoplasmic reticulum stress, atherosclerosis and chronic kidney disease associated with SREBP expression changes. In the liver, SREBPs are involved in the pathogenesis of nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, hepatitis and hepatic cancer. There are several SREBP inhibitors that have potential for treating obesity, diabetes and cancer. This review assesses the recent findings about the roles of SREBPs in the physiology of organs’ function and pathogenesis of liver diseases.
Despite all the new treatments, metastatic breast cancer (BC) causes many deaths. Chlorogenic acid (CGA) is a polyphenol compound with various pharmacological traits, such as anticancer properties. Targeting apoptotic death pathways has been propounded as the most effective therapeutic method in various cancers. In the current study, apoptotic agents such as p53, Bax, Bcl‐2, and caspase‐3 have been investigated. The experimental groups included saline, BC, CGA, protective (PR), and treatment (TM) groups. First, 4T1 mouse BC was established and then the effects of treatment with CGA were investigated through measurement of tumor weight and volume, metastatic nodules, liver biochemical tests, hematoxylin and eosin (H&E), immunohistochemistry (IHC) staining, and real‐time reverse transcription‐polymerase chain reaction (RT‐PCR) in experimental groups. The findings showed that CGA reduced tumor weight and volume in the PR group (P < .05) and in the TM group (P < .001). Surprisingly, it eliminated the tumors in the TM group. Metastatic nodules in the PR and TM groups were significantly reduced as compared with the BC group (P < .001). The evaluation by H&E staining showed cell apoptosis in both the PR and TM groups. The results of real‐time RT‐PCR showed that CGA therapy increased the expression ratio of Bax/Bcl‐2 (P < .001 and P < .05, respectively) and the expression of p53 (P < .001 and P < .05, respectively) and caspase‐3 genes (P < .01) in the PR and TM groups. The IHC data regarding the Bax/Bcl‐2 ratio confirmed the other results (P < .001). The findings demonstrate that CGA plays a significant role in the induction of apoptosis and the treatment of 4T1 BC tumors in BALB/c mice.
Ghrelin is a gut hormone shown to have protective effects throughout the gastrointestinal tract. This study aims to investigate its protective effect in celiac disease induced in rats. Twenty-four rat pups were divided into 4 groups as follows: control, disease (1.5 mg/g intragastric gliadin), co-treatment (50 ng/g intraperitoneal ghrelin after gliadin gavage) and pretreatment (50 ng/g intraperitoneal ghrelin before gliadin gavage). Animals' weight gain was charted. Histological features assessed include villus length, villus width, crypt depth and number of intraepithelial lymphocytes. Tissue interferon-gamma was quantified by ELISA. ANOVA was used to compare results statistically. Results showed that villi were shortened in the diseased group, but were as long as the control in pretreatment and co-treatment groups. Crypt depth had increased in disease group, but turned to normal in co-treatment group. Number of intraepithelial lymphocytes was significantly higher in disease group than the control, while no difference was observed between co-treatment and control groups. Disease and control animals weighed equally at the end of the experiment, but ghrelin-treated animals had significantly gained more weight than these two. Interferon-gamma measurement revealed no significant difference among groups. We concluded administration of ghrelin led to histological improvement of celiac disease which was more obvious if administered after exposure to gliadin.
Purpose
Gastritis is found to be one of the most common gastrointestinal diseases worldwide. However, current therapeutic agents cause side effects, interaction, and recurrence. Allantoin has anti-inflammatory and wound healing properties. In this study, the therapeutic effect of allantoin has been assessed on the histopathological indices and gastric mucosal barrier of male rats.
Methods
Male rats were equally divided into control, ethanol-induced gastritis, and allantoin groups. The therapeutic groups consisted of gastritis plus 12.5 mg/kg allantoin, gastritis plus 25 mg/kg allantoin, and gastritis plus 50 mg/kg allantoin groups. After 5 days of allantoin administration, the rats were sacrificed and a part of their gastric tissue was maintained at −70 °C for prostaglandin E2 (PGE2) and non-protein sulfhydryl (NP-SH) measurements. Another part was stained with hematoxylin and eosin and Masson’s trichrome.
Results
We found that Allantoin increased parietal and mucosal cell counts and mucosal thickness after gastritis induction. In addition, the number of leukocytes and vessels decreased in both of the mucosal and the submucosal layers. Allatoin improved gastric ulcer in all treatment groups. Gastric levels of PGE2 and NP-SH increased after allantoin treatment.
Conclusion
This study indicated that allantoin had a considerable effect on gastritis treatment, which seems to result from the reinforcement of gastric mucosal barrier.
Objectives
Diabetes mellitus is one of the most common metabolic diseases. Tropisetron, as a 5-HT3 receptor antagonist, has a considerable role in the inflammation and oxidative stress lowering. This study aimed to investigate the effect of this 5-HT3 receptor antagonist on insulin secretion in male diabetic rats and the possible mechanisms.
Methods
Animals were divided into five equal groups; the control, tropisetron, diabetes, tropisetron–diabetes and glibenclamide–diabetes (7 in each group). Tropisetron and glibenclamide were administrated for 2 weeks after inducing type 1 diabetes.
Key findings
We demonstrated that insulin secretion improved robustly in diabetes–tropisetron compared with the diabetic group. Oxidative stress biomarkers were lower in a diabetes–tropisetron group than in diabetic rats. Simultaneously, tropisetron administration promoted the expression of ZnT8 and GLUT2 and also beta-cell mass in pancreatic tissue, while the expression of uncoupling protein 2 (UCP2) was restrained. The histological evaluation confirmed our results. These effects were equipotent with glibenclamide, indicating that tropisetron can protect islets from the abnormal insulin secretion and morphological changes induced by type 1 diabetes.
Conclusions
This effect might be partly related to the modulated UCP2/ZnT8 signal pathway and improved oxidative stress-induced damage.
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