Tissue & cell最新文献

Background: Ulcerative colitis (UC) is a lifelong chronic inflammatory disease that is characterized by the absence of specific markers for diagnosis and prognosis. TPM3 is an integral component of the thin filament, responsible for the structural stability of actin filaments and modulation of cytoskeletal function. This study investigated the regulatory role of TPM3 in UC and its potential mechanisms.

Methods: At the clinical level, TPM3 levels were assessed in serum and mucosal tissues of UC and other enteric disease. At the cellular level, the effects of TMP3 overexpressing lentivirus on Caco-2 cell phenotype and the barrier of IL-1β-induced UC model were explored. At the animal level, the effects of TMP3 overexpressing lentivirus on symptoms and colonic damage in a DSS-induced UC model were explored.

Results: TPM3 expression in serum of UC patients was significantly lower than that of other enteric disease, and TPM3 levels in the intestinal mucosa showed a negative correlation with the Mayo score of UC patients. TPM3 overexpression alleviates IL-1β-induced apoptosis and inhibition of invasion and migration in UC model in vitro. In monolayer Caco-2 cells, TPM3 overexpression rescued the IL-1β-induced decrease in transepithelial electrical resistance and tight junction markers (ZO-1 and Occludin) and increase in permeability. In animal experiments, TPM3 overexpression increased body weight and colon length and decreased disease activity index in a DSS-induced UC model. In tissue staining, it alleviated pathological damage and upregulated Occuludin and TPM3 levels in the colon.

Conclusion: TPM3 levels correlated with UC disease course and TPM3 overexpression alleviated symptoms/phenotypes and barrier damage in UC models in vivo and in vitro. TPM3 may serve as a potential novel biomarker for UC diagnosis and prognosis.

Purpose: Dermal cells fabricate and interact with the extracellular matrix to preserve structural integrity and further healthy function during wound healing. Collagen is a critical component of the matrix, challenging collagen's stability during wound injury. Natural sources especially plant extracts can promote wound healing and interact with collagen to increase its action. In this context, we studied the effect of extracted fish and bovine collagen in controlling cell proliferation, migration, and adhesion in dermal cells pretreated with plant extract.

Methods: An acid-solubilization procedure was used to extract collagen fish (CF) and bovine (CB). Three different hydro-ethanolic extracts were prepared Pistacia lentiscus leaves (PL), Calendula officinalis leaves (FL), and flowers (FS). Migration potency was determined using scratch assay. The covered surface area was estimated after 16 hours and 24 hours after cell seeding. The chemotaxis was determined by the Boyden chamber, and the film was coated with CF or CB (10 µg/mL). or poly-L-lysine (50 µg/mL).

Findings: We show that CF and CB increase adherence and migration of 3T3-L1 cells, which are pretreated with PL, FL, and FS. In addition, we highlighted a significantly higher cell adhesion on the CF matrix compared to CB. However, in the case of cells pre-treated with PL, the attachment to CF and CB increased significantly compared to untreated cells. The exposition of Hacat cells to plant extracts regulates the secretion of MMP2 and MMP and the production of reactive oxygen species.

Conclusion: CF and CB promote higher migration and adhesion of dermal cells pre-treated with wound-healing herbal extracts. In future studies, composite dressings based on collagen, P. lentiscus, and C. officinalis extracts can potentially be developed for tissue regeneration.

Background: Our purpose is to explore the influence of Hua Yu Xiao Zheng (HYXZ) decoction on the senescence of ectopic endometrial stromal cells (ESCs) in endometriosis as well as its relevant mechanisms.

Methods: The proliferation, apoptosis, migration, and invasion of primary ectopic ESCs was assessed utilizing EdU assay, flow cytometry, and transwell assays. Moreover, the effects of HYXZ decoction on oxidative stress were evaluated using DCFH-DA probe and via measuring MDA, GSH, SOD and GPx levels. The function of HYXZ decoction on cell senescence were explored through utilizing SA-β-gal staining and measuring the cumulative population doubling level and the average telomere length. The protein expression was measured using western blotting analysis. Endometriosis in rats was surgically induced, and the efficacy and mechanism of HYXZ decoction were determined in vivo.

Results: HYXZ decoction inhibited the growth, migration, and invasion of ectopic ESCs, but induced oxidative stress and senescence. HYXZ decoction inhibited PI3K/AKT signaling in ectopic ESCs. PI3K-AKT signaling pathway activator (740Y-P) significantly reversed the inhibitory effects of HYXZ decoction on ectopic ESCs. In rats with endometriosis, oral administration of HYXZ decoction inhibited lesion volume alone with the increased oxidative stress and cell senescence, as well as the decreased PI3K/AKT activity.

Conclusion: HYXZ decoction might repress the growth and migration of ectopic ESCs, and induce oxidative stress and senescence through suppressing PI3K/AKT signaling. This finding indicates that HYXZ decoction may be a potential therapeutic drug against endometriosis.

Background: We aimed to explore the biological function of CLMP in colorectal cancer (CRC) and to determine the effect of CLMP on 5-fluorouracil (5-FU) sensitivity in CRC.

Methods: Sixteen pairs of CRC tissues and paracancerous tissues were collected. Immortalized intestinal epithelial cell lines and human CRC cell lines were purchased, and the cells were treated with DMSO and 5-FU. RTqPCR, western blotting, CCK8, colony formation, scratch, and Transwell assays were performed to determine the molecular mechanism of CLMP in the regulation of autophagy and sensitivity to 5-FU in CRC cells.

Results: CLMP was expressed at low levels in CRC tissues. The upregulation of CLMP expression could inhibit cell proliferation, colony number, migration and invasion and increase the sensitivity of CRC cells to 5-FU. Mechanistic studies revealed that the overexpression of CLMP could block the activation of the PI3K/AKT signaling pathway, inhibit autophagy, and increase the chemosensitivity of CRC cells to 5-FU.

Conclusion: CLMP overexpression can reduce the level of autophagy and increase the sensitivity of CRC to 5-FU, providing a potential target for the treatment of CRC.

Sharks and rays present an osmoregulatory mechanism essentially exercised by a rectal salt gland. Histological assessments of this gland, however, are notoriously lacking. In this sense, histological assessments of the rectal gland of the Brazilian guitarfish, Pseudobatos horkelii obtained from off the coast of Rio de Janeiro, Brazil, were carried out herein. Rectal gland samples were histologically processed with hematoxylin/eosin and special Masson's Trichrome stain. Three main regions were identified: the capsule, secretory parenchyma and central duct. Highly vascularized connective tissue was observed in the capsular region, surrounded by a superficial epithelium composed of a layer of cubic cells. Lymphoid tissue was present outside the capsule. The capsule presented connective tissue invaginations, forming interlobular septa. Each septum, surrounded by fibroelastic tissue, delimited the secretory lobes filled with secretory tubules, whose lumens exhibited a larger diameter and a greater number of secretory cells as they approached the central duct. The duct to which the organ's secretory tubules open, at the center of the rectal gland, presents a lumen lined with stratified epithelium, containing acidophilic intraepithelial and mucous cells. Most analyzed morphological characteristics are in accordance with morphological aspects reported in previous ray studies concerning other species presenting similar phylogeny, habitat and feeding characteristics as P. horkelii. These assessments are paramount in understanding species-specific osmoregulation and informing conservation strategies, particularly for threatened species like the Brazilian guitarfish.

Background: Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by memory impairment and cognitive decline. Our previous research has demonstrated that pathological Tau and Amyloid-beta (Aβ) disrupt autophagy gene expression, independently. Other studies have shown that these pathological aggregates create a vicious cycle with oxidative stress.

Methods: In the current research, the effect of Tau and Amyloid-beta was compared on behavioral function, autophagy gene dysfunction, and oxidative stress in the Drosophila model for AD. Thymoquinone (TQ), an antioxidant agent, was then tested to examine if it could ameliorate the adverse effects of Tau and Amyloid-beta. In addition, the impact of TQ on Tau aggregation was investigated in vitro.

Results: Our data showed that Tau and Amyloid-beta induced behavioral disability, autophagy gene dysregulation, and oxidative stress. TQ treatment significantly improved conditions in both types of transgenic flies, with a more profound alleviation in Tau transgenic flies, despite tau having a greater impact on autophagy gene dysregulation. Furthermore, TQ prevented the aggregation of Tau in vitro.

Conclusion: To sum up, Tau may exert its toxic effect on autophagy and behavioral dysfunctions significantly through oxidative stress while Amyloid-beta may confer its toxicity through multiple pathways, including oxidative stress. Moreover, since TQ ameliorates the adverse effect of tau and amyloid beta, it could be considered a promising approach for treating AD, probably in combination with other medications against Aβ or Tau.

A variety of biological functions is attributed to the renin-angiotensin system (RAS). One of them is regulating vascular tone through its final effector Angiotensin II (Ang II). Ang II action is mediated by the Angiotensin type 1 receptor (AT1-R) which plays a role in vasoconstriction, and Angiotensin type 2 receptor (AT2-R) which may result in vascular relaxation through the releasing of endothelium mediates relaxation factors such as Nitric Oxide (NO). Therefore, this study investigated the role of AT2-R in vasodilation after blocking the effect of AT1-R in the rat aorta. Furthermore, it is to determine whether or not Ang II through NO has a role in rat aorta dilation via using valsartan. For control isolated aortic rings were preincubated with Valsartan (AT1- R inhibitor) and then stimulated with angiotensin II dose-dependent. For treating aortic rings different blockers and inhibitors were used. Pd123177 (AT2- R inhibitor) (20 µM), an inhibitor of PKA H-89 (10 µM), eNOS inhibitor L-NAME (0.3 mM), with group of K channel blockers such as TEA (1 mM), 4-AP (1 mM), BaCl2 (1 mM), clotrimazole (0.03 mM) and GLIB (0.01 mM). Our analysis demonstrates vasodilation in aortic rings induced by Ang II after blocking ATI-R and this response was highly reliant on PKA/eNOS and cyclic guanosine monophosphate (cGMP). The data from this investigation provided evidence that Ca2 + activated K+ channels (KCa) and Voltage-dependent K channel (KV) mediated Ang II vasorelaxation. Finally, these results indicate that angiotensin II primarily induces dilatation AT2-R after inhibiting the angiotensin AT1 receptor through a cascade of signaling pathways involving many enzymes and plasma membrane protein channels.