Publications by authors named "Jinlai Gao"

Background: To explore the clinical characteristics of ovarian Brenner tumors and provide some basis for the treatment regimen of ovarian Brenner tumors.

Methods: A retrospective analysis of the pathology database of surgical specimens at the Huzhou Maternal and Child Health Hospital from September 2008 to February 2023 was conducted. Patients who were pathologically diagnosed with ovarian Brenner tumors were included.

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Pathological cardiac hypertrophy can lead to heart failure, making its prevention crucial. SOX4, a SOX transcription factor, regulates tissue growth and development, although its role in pathological cardiac hypertrophy is unclear. We found that the SOX4 expression was elevated in hypertrophic hearts and angiotensin II (Ang II)-treated neonatal rat cardiomyocytes (NRCMs), and knocking down the SOX4 expression in NRCMs and mouse hearts significantly reduced the hypertrophic response.

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Background: Bladder cancer, predominantly affecting men, is a prevalent malignancy of the urinary system. Although platinum-based chemotherapy has demonstrated certain enhancements in overall survival when compared to surgery alone, the efficacy of treatments is impeded by the unfavorable side effects of conventional chemotherapy medications. Nonetheless, immunotherapy exhibits potential in the treatment of bladder cancer.

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Recently, PI3K and HDAC have been considered as promising targets for the cancer therapy. A couple of pan-PI3K/HDAC dual inhibitors have been developed as a new class of anticancer agents. Herein, we discovered a new series of (S)-N-(thiazol-2-yl) pyrrolidine-1,2-dicarboxamide derivatives targeting PI3Kα/HDAC6.

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Excess levels of chemical hepatotoxicants (alcohol, aflatoxin B1), oxidative drugs (acetaminophen) and some cytokines (ET-1, TGF-β1) can induce chronic or acute liver injury. After these, the severe hepatic disease, especially the liver fibrosis (LF) occurs without taking measures, which brings threat to human health. The dibenzocyclooctadiene lignans of S.

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Herein, we report a distinctive photoredox/copper dual-catalyzed esterification of benzylic C-H bonds through the combination of photoredox-mediated hydrogen atom transfer and Cu(II)-mediated radical-polar crossover. This methodology demonstrates a high functional group tolerance (>40 examples) and moderate to good yields with structurally diverse benzylic C-H substrates. Notably, stoichiometric amounts of carboxylic acids are used as coupling partners, which allows the synthesis of structurally diverse benzylic esters and the late-stage functionalization of pharmaceuticals.

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Background: It is critical to develop a reliable and cost-effective prognostic tool for colorectal cancer (CRC) stratification and treatment optimization. Tumor-stroma ratio (TSR) may be a promising indicator of poor prognosis in CRC patients. As a result, we conducted a systematic review on the predictive value of TSR in CRC.

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Purpose: To evaluate the effects of manganese superoxide dismutase (Mn-SOD) from thermophilic bacterium HB27 (name as Tt-SOD) on chemical cystitis.

Methods: Control and experimental rats were infused by intravesical saline or hydrochloric acid (HCl) on the first day of the experiments. Saline, sodium hyaluronate (SH) or Tt-SOD were infused intravesically once a day for three consequent days.

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Article Synopsis
  • A study explored the effects of superoxide dismutase (SOD) from a thermophilic bacterium on chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) using a rat model.
  • The treatment with Tt-SOD improved inflammation and fibrosis in the prostate, increased pain thresholds, and showed an anti-inflammatory response by reducing inflammatory cytokines and enhancing antioxidant levels.
  • Tt-SOD worked by modulating key proteins involved in inflammation, suggesting it could be a potential therapeutic option for patients suffering from CP/CPPS.
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The heart is a high energy demand organ and enhancing mitochondrial function is proposed as the next-generation therapeutics for heart failure. Our previous study found that anthelmintic drug niclosamide enhanced mitochondrial respiration and increased adenosine triphosphate (ATP) production in cardiomyocytes, therefore, this study aimed to determine the effect of niclosamide on heart failure in mice and the potential molecular mechanisms. The heart failure model was induced by transverse aortic constriction (TAC) in mice.

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Melanoma is a common type of cutaneous tumor, but current drug treatments do not satisfy clinical practice requirements. At present, mitochondrial uncoupling is an effective antitumor treatment. Triclosan, a common antimicrobial, also acts as a mitochondrial uncoupler.

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Article Synopsis
  • * The study aims to create a more effective delivery method by synthesizing pegylated niclosamide (mPEG5000-Nic), which significantly enhances solubility and decreases toxicity while showing promise against colon cancer cells both in lab settings and in animal models.
  • * The results indicate that mPEG5000-Nic successfully inhibits tumor growth in a mouse model without causing noticeable adverse effects, suggesting it could be a viable option for cancer treatment compared to traditional therapies like 5
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Cardiomyocyte loss and cardiac fibrosis are the main characteristics of cardiac ischemia and heart failure, and mitochondrial function of cardiomyocytes is impaired in cardiac ischemia and heart failure, so the aim of this study is to identify fate variability of cardiomyocytes and cardiac fibroblasts with mitochondria inhibition and explore the underlying mechanism. The mitochondrial respiratory function was measured by using Oxygraph-2k high-resolution respirometry. The STAT3 expression and activity were evaluated by western blot.

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Induction of mild mitochondrial uncoupling is protective in a variety of disorders; however, it is unclear how to recognize the mild mitochondrial uncoupling induced by chemical mitochondrial uncouplers. The aim of the present study is to identify the pharmacological properties of mitochondrial uncoupling induced by mitochondrial uncouplers in cardiomyocytes. Neonatal rat cardiomyocytes were cultured.

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Background And Purpose: The anti-helminthic drug niclosamide regulates multiple cellular signals including STAT3, AMP-activated protein kinase (AMPK), Akt, Wnt/β-catenin and mitochondrial uncoupling which are involved in neointimal hyperplasia. Here we have examined the effects of niclosamide on vascular smooth muscle cell proliferation, migration and neointimal hyperplasia and assessed the potential mechanisms.

Experimental Approach: Cell migration was measured by using wound-induced migration assay and Boyden chamber assay.

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  • Researchers investigated how inhibiting mitochondrial fission affects vasoconstriction caused by endothelin-1, a molecule linked to hypertension.
  • They found that the inhibitor mdivi-1 relaxed artery constriction induced by endothelin-1 in rat mesenteric arteries and thoracic aorta, highlighting its potential therapeutic role.
  • The study concluded that endothelin-1 enhances mitochondrial fission in vascular smooth muscle cells, and using mitochondrial fission inhibitors can help reduce this constriction.
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We previously demonstrated that the typical mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) inhibited artery constriction, but CCCP was used only as a pharmacological tool. Niclosamide is an anthelmintic drug approved by FDA. Niclosamide ethanolamine (NEN) is a salt form of niclosamide and has been demonstrated to uncouple mitochondrial oxidative phosphorylation.

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Article Synopsis
  • * The study found that using mitochondrial fission inhibitors, like mdivi-1, reduced constriction caused by agents like phenylephrine and high potassium levels in rat arteries.
  • * Mitochondrial fission was linked to increased oxidative stress and calcium levels in smooth muscle cells, suggesting that controlling mitochondrial dynamics could influence arterial constriction and overall vascular function.
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Unlabelled: Colon-targeted drug delivery and circumventing drug resistance are extremely important for colon cancer chemotherapy. Our previous work found that dimethyl fumarate (DMF), the approved drug by the FDA for the treatment of multiple sclerosis, exhibited anti-tumor activity on colon cancer cells. Based on the pharmacological properties of DMF and azo bond in olsalazine chemical structure, we designed azo polymeric micelles for colon-targeted dimethyl fumarate delivery for colon cancer therapy.

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  • The study investigates how the mitochondrial uncoupler CCCP affects blood vessel function in rat arteries and aims to understand the underlying mechanisms.
  • CCCP was found to relax artery constriction caused by certain stimuli and prevents constriction through various cellular changes, including increasing the ADP/ATP ratio and activating AMPK.
  • The results suggest that CCCP induces relaxation of blood vessels through non-potassium channel mechanisms, highlighting potential applications for vascular health.
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GDF11/BMP11, a member of TGF-β superfamily, was reported to rejuvenate heart, skeletal muscle and blood vessel architecture in aged mice. However, the rejuvenative effects of GDF11 were questioned recently. Here, we investigated the effects of GDF11 on smad and non-smad signals in human umbilical vein endothelial cells (HUVECs) and the effects of GDF11 on proliferation and migration of HUVECs and primary rat aortic endothelial cells (RAECs).

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The bile acids (BAs) and their conjugates have vascular activities and the serum levels of BAs and their conjugates are increased in liver diseases. In the present study, we examined the in vitro vasoactivities of BAs conjugates taurochenodeoxycholate (TCDC) (5-80 µM), glycochenodeoxycholate (GCDC) (20-150 µM) and tauroursodeoxycholate (TUDC) (20-150 µM) in rat mesenteric arteries and thoracic aorta. The isometric tension of rat mesenteric arteries and thoracic aorta was recorded by using multi-wire myograph systems.

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Background And Purpose: Dimethyl fumarate (DMF) is a newly approved drug for the treatment of relapsing forms of multiple sclerosis and relapsing-remitting multiple sclerosis. Here, we investigated the effects of DMF and its metabolites mono-methylfumarate (MMF and methanol) on different gastrointestinal cancer cell lines and the underlying molecular mechanisms involved.

Experimental Approach: Cell viability was measured by the MTT or CCK8 assay.

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