Last update 01 Nov 2024

caspase 8 x caspase 3 x caspase 9

Last update 01 Nov 2024

Basic Info

Related Targets

caspase 8caspase 3caspase 9

Drugs associated with caspase 8 x caspase 3 x caspase 9

NO-Ursodeoxycholic Acid

Target

caspase 3 x caspase 8 x caspase 9

Mechanism

caspase 3 inhibitors [+2]

Active Org.-

Originator Org.

Nicox SA

Active Indication-

Inactive Indication

Hypertension, Portal

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with caspase 8 x caspase 3 x caspase 9

NCT05292872 / CompletedNot Applicable

Replicate Studies Evaluating the Effectiveness of Obeticholic Acid on Hepatic Real-World Outcomes in Patients With Primary Biliary Cholangitis

This is an observational, retrospective cohort study of patients with primary biliary cholangitis (PBC) who failed ursodeoxycholic acid (UDCA) treatment, using a real-world data source, the Komodo Health United States (US) claims database. The study is designed to evaluate the effectiveness of obeticholic acid (OCA). All patients who meet diagnostic criteria for PBC in the database between 01 Jun 2015 and 31 Dec 2021 and who meet all eligibility criteria will be considered for this study.

Start Date28 Mar 2022

Sponsor / Collaborator

Intercept Pharmaceuticals, Inc.

[+2]

NCT03512821 / CompletedPhase 1

A Single-dose, Comparative Bioavailability Study of Two Formulations of Ursodiol 500mg Tablets Under Fed Conditions

single-dose, comparative bioavailability study of two formulations of ursodiol 500mg tablets under fed conditions

Start Date01 Oct 2017

Sponsor / Collaborator

Daewoong Pharmaceutical Co., Ltd.

100 Clinical Results associated with caspase 8 x caspase 3 x caspase 9

100 Translational Medicine associated with caspase 8 x caspase 3 x caspase 9

0 Patents (Medical) associated with caspase 8 x caspase 3 x caspase 9

2,457

Literatures (Medical) associated with caspase 8 x caspase 3 x caspase 9

01 Jan 2025·Journal of Ethnopharmacology

Dehydrocorydaline attenuates myocardial ischemia-reperfusion injury via the FoXO signalling pathway: A multimodal study based on network pharmacology, molecular docking, and experimental study

Article

Author: Chen, Keji ; Chen, Daxin ; Meizhu, Wu ; Yu, Zikai ; Shen, Aling ; Renfeng, Li ; Zhi, Guo ; Li, Mengfan ; Hua, Qu ; Zucheng, Shang ; Zikai, Yu ; Guo, Zhi ; Yang, Wenwen ; Qu, Hua ; Li, Hongzheng ; Daxin, Chen ; Aling, Shen ; Hongzheng, Li ; Lu, Yingdong ; Li, Renfeng ; Wenwen, Yang ; Changgeng, Fu ; Lin, Guosheng ; Shang, Zucheng ; Yingdong, Lu ; Keji, Chen ; Mengfan, Li ; Fu, Changgeng ; Guosheng, Lin ; Wu, Meizhu

ETHNOPHARMACOLOGICAL RELEVANCEDehydrocorydaline (DHC), an active component of Corydalis yanhusuo (Y.H. Chou & Chun C. Hsu) W.T. Wang ex Z.Y. Su & C.Y. Wu (Papaveraceae), exhibits protective and pain-relieving effects on coronary heart disease, but the underlying mechanism still remains unknown.AIM OF THE STUDYNetwork pharmacology and experimental validation both in vivo and in vitro were applied to assess whether DHC can treat myocardial ischemia-reperfusion injury (MIRI) by regulating the forkhead box O (FoxO) signalling pathway to inhibit apoptosis.MATERIALS AND METHODSDHC and MIRI targets were retrieved from various databases. Molecular docking and microscale thermophoresis (MST) determined potential binding affinity. An in vivo mouse model of MIRI was established by ligating the left anterior descending coronary artery. C57BL/6N mice were divided into sham, MIRI, and DHC (intraperitoneal injection of 5 mg/kg DHC) groups. Haematoxylin and eosin, Masson, and immunohistochemical stainings verified DHC treatment effects and the involved signalling pathways. In vitro, H9c2 cells were incubated with DHC and underwent hypoxia/reoxygenation. TUNEL, JC-1, and reactive oxygen species stainings and western blots were used to explore the protective effects of DHC and the underlying mechanisms.RESULTSVenny analysis identified 120 common targets from 121 DHC and 23,354 MIRI targets. DHC exhibited high affinity for CCND1, CDK2, and MDM2 (<-7 kcal/mol). In vivo, DHC attenuated decreases in left ventricular ejection fraction and fractional shortening, reduced infarct sizes, and decreased cTnI and lactate dehydrogenase levels. In vitro, DHC alleviated apoptosis and oxidative stress in the hypoxia/reoxygenation model by attenuating ΔΨm disruption; reducing the production of reactive oxygen species; upregulating Bax and CCND1 via the FoxO signalling pathway, as well as cleaved-caspase 8; downregulating the apoptosis-associated proteins Bcl-2, Bid, cleaved-caspase 3, and cleaved-caspase 9; and promoting the phosphorylation of FOXO1A and MDM2.CONCLUSIONBy upregulating the FoxO signaling pathway to inhibit apoptosis, DHC exerts a cardioprotective effect, which could serve as a potential therapeutic option for MIRI.

31 Dec 2024·Annals of Medicine

Propyl gallate induces human pulmonary fibroblast cell death through the regulation of Bax and caspase-3

Article

Author: Park, Woo Hyun

Propyl gallate (PG) has been found to exert an inhibitory effect on the growth of different cell types, including lung cancer cells. However, little is known about the cytotoxicological effects of PG specifically on normal primary lung cells. The current study examined the cellular effects and cell death resulting from PG treatment in human pulmonary fibroblast (HPF) cells. DNA flow cytometry results demonstrated that PG (100-1,600 μM) had a significant impact on the cell cycle, leading to G1 phase arrest. Notably, 1,600 μM PG slightly increased the number of sub-G1 cells. Additionally, PG (400-1,600 μM) resulted in the initiation of cell death, a process that coincided with a loss of mitochondrial membrane potential (MMP; ΔΨm). This loss of MMP (ΔΨm) was evaluated using a FACS cytometer. In PG-treated HPF cells, inhibitors targeting pan-caspase, caspase-3, caspase-8, and caspase-9 showed no significant impact on the quantity of annexin V-positive and MMP (ΔΨm) loss cells. The administration of siRNA targeting Bax or caspase-3 demonstrated a significant attenuation of PG-induced cell death in HPF cells. However, the use of siRNAs targeting p53, Bcl-2, or caspase-8 did not exhibit any notable effect on cell death. Furthermore, none of the tested MAPK inhibitors, including MEK, c-Jun N-terminal kinase (JNK), and p38, showed any impact on PG-induced cell death or the loss of MMP (ΔΨm) in HPF cells. In conclusion, PG induces G1 phase arrest of the cell cycle and cell death in HPF cells through apoptosis and/or necrosis. The observed HPF cell death is mediated by the modulation of Bax and caspase-3. These findings offer insights into the cytotoxic and molecular effects of PG on normal HPF cells.

01 Nov 2024·Fish & Shellfish Immunology

β-glucan regulates the intestinal immunity of pearl gentian grouper via the nuclear factor kappa B signaling pathway

Article

Author: Lu, Yishan ; Wang, Fan ; Xu, Jia ; Shen, Peihong ; Lai, Junxiang ; Hu, Chaoqun ; Jiang, Fajun

The preceding study observed that yeast β-glucan supplementation enhanced intestinal health and augmented disease resistance in pearl gentian grouper (Epinephelus lanceolatus♂ × Epinephelus fuscoguttatus♀), which occurred concurrently with the activation of the nuclear factor kappa B (NFκB) signaling pathway. Thus, we hypothesized that β-glucan improves intestinal health in grouper by modulating the NFκB pathway. Accordingly, the present study examined the effects of NFκB pathway disruption using a specific inhibitor on the intestinal health of pearl gentian grouper that had been injected with β-glucan. The experimental groups were as follows, (1) CD group: PBS injected; (2) βG group: β-glucan injected at a dose of 80 mg/kg; (3) PDTC group: NFκB inhibitor PDTC injected at a dose of 30 mg/kg; (4) βG + PDTC group: a combination of β-glucan (80 mg/kg) and PDTC (30 mg/kg) injected together. The results demonstrated that β-glucan-induced increases in mRNA expression levels of NFκB inhibitor α (iκbα) and p65, the degradation and phosphorylation of IκBα, and the phosphorylation of NFκB p65 were significantly inhibited following NFκB inhibition using PDTC in the intestine of grouper. The PDTC injection resulted in a significant reduction in the β-glucan-induced increase in mucin levels. The β-glucan-induced elevation of alkaline phosphatase (AKP) activity, component 3 (C3) content, and inflammatory factors were significantly suppressed following NFκB inhibition. The βG + PDTC treatment resulted in a restoration of catalase (CAT) enzyme activity to the level observed in the CD treatment, while total antioxidant capacity (T-AOC) was decreased to the level of the βG treatment. The β-glucan-induced downregulation of caspase8 (casp8) was reversed following NFκB inhibition, as well as the mRNA levels of casp3 and casp9 being elevated to a greater extent. In conclusion, the β-glucan-regulated intestinal immunity in grouper may be mediated by the NFκB pathway. Furthermore, the inhibitory effect of β-glucan on apoptosis and oxidative stress may not be related to the NFκB signaling pathway.

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