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Topical Vitamin D Analogs
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
It has been suggested that apoptosis is an important mechanism in the vitiligo pathogenesis. A variety of factors, including immune cytokines, some environmental chemicals, and/or other molecular mechanisms induce apoptosis. Because of that, it can be assumed that anti-apoptotic therapy might be able to prevent or to stop the progression of the disease [6]. As a medical therapy, vitamin D is a good alternative because it reduces the apoptotic activity induced by UVB in keratinocytes and melanocytes [17,18].
In Silico approach of soursop leaf for prediction of anticancer molecular target therapy
Published in Ade Gafar Abdullah, Isma Widiaty, Cep Ubad Abdullah, Medical Technology and Environmental Health, 2020
M.K. Dewi, Y. Kharisma, L. Yuniarti
Apoptosis is one of the targets of cancer treatment. The success of cancer therapy depends mainly on the ability of therapy to induce apoptosis through the mechanism of increasing expression of genes that induce apoptosis, as well as inhibiting genes that inhibit apoptosis (Hassan et al. 2014).
Basic science of endometriosis
Published in Caroline Overton, Colin Davis, Lindsay McMillan, Robert W Shaw, Charles Koh, An Atlas of ENDOMETRIOSIS, 2020
Caroline Overton, Colin Davis, Lindsay McMillan, Robert W Shaw, Charles Koh
The endometrial fragments in menstrual effluent are composed of necrotic and living cells, which do not survive in ectopic locations because of programmed cell death. Augmented cell survival has been shown in eutopic endometrium from women with endometriosis. Cell death by apoptosis is reduced and cell proliferation increased. These changes may facilitate invasion of the endometrium7.
Ameliorative effect of gallic acid on cisplatin-induced ovarian toxicity in rats
Published in Drug and Chemical Toxicology, 2023
Elif Ayazoglu Demir, Ahmet Mentese, Ayten Livaoglu, Nihal Turkmen Alemdar, Selim Demir
Apoptosis is a physiologically controlled cell death mechanism and plays an important role in ensuring the integrity of the organism by eliminating injured or damaged cells. However, an uncontrolled and untimely apoptosis causes tissue damage (Kaygusuzoglu et al.2018). Caspase-3 plays an important role in driving apoptosis. Since caspase-3 activation is an irreversible step that induces apoptosis, it is frequently used in studies to evaluate apoptosis (Altindag and Meydan 2021). In the present study, increased levels of caspase-3 were observed in CDDP group compared to the control group. This finding indicates that CDDP activates apoptotic processes on ovarian tissue. Treatments of GA exhibited strong antioxidant and anti-inflammatory properties, which protect ovarian tissue by decreasing the caspase-3 levels. Similarly, Kilic et al. (2019) reported that GA inhibits the CDDP-induced ototoxicity in rats via decreasing the MDA and caspase-3 levels and increasing superoxide dismutase and glutathione peroxidase levels. Recently, Altindag and Meydan (2021) demonstrated that GA has testicular protective effect in a cisplatin-induced injury model via decreasing the MDA, 8-OHdG, caspase-3 levels and increasing the CAT levels.
Delivery of human natural killer cell-derived exosomes for liver cancer therapy: an in vivo study in subcutaneous and orthotopic animal models
Published in Drug Delivery, 2022
Ho Yong Kim, Hyun-Ki Min, Hyeong-Woo Song, Ami Yoo, Seonmin Lee, Kyu-Pyo Kim, Jong-Oh Park, You Hee Choi, Eunpyo Choi
Apoptosis can be initiated through one of two pathways. In the intrinsic pathway, perforin (membrane disrupting protein) and granzyme B (serine protease) are secreted by exocytosis; they induce apoptosis via cytochrome c release (Metkar et al., 2002; Trapani & Smyth, 2002; Voskoboinik et al., 2006). In the extrinsic pathway, target cell death ligands (FasL and TRAIL) bind to their cognate receptors (Fas and TRAIL-R1/TRAIL-R2) (Zamai et al., 1998; Ferguson & Griffith, 2007). Both pathways involve the activation of apoptotic cysteine proteases (caspases) (Xu & Shi, 2007; Green & Llambi, 2015). In the intrinsic pathway, perforin and granzyme B induce the release of cytochrome c, which then activates caspase 9. In the extrinsic pathway, FasL and TRAIL activate caspase 8, followed by caspase 3 or caspase 7. This subsequently activates PARP in both pathways. As shown in Figure 5, NK-exo induced the apoptosis of Hep3B cells in a dose-dependent manner. Here, to evaluate the signaling pathway of apoptotic effects in Hep3B cells, we assessed the expressions of caspases and PARP using western blot analysis. Apoptosis effectors, caspases, and PARP activation are performed by cleavage. NK-exo increased the cleaved caspase (-3, -7, -8, and -9), cleaved PARP, and cytochrome c expression in a dose-dependent manner (Figure 7(A,B)). In addition, the cytotoxic proteins-induced apoptosis (e.g. perforin, granzyme B, FasL, and TRAIL) were increased in a dose-dependent manner (Figure 7(A,C)).
Insulin-like growth factor-1 reduces hyperoxia-induced lung inflammation and oxidative stress and inhibits cell apoptosis through PERK/eIF2α/ATF4/CHOP signaling
Published in Experimental Lung Research, 2022
Haixia Cui, Shujian Zhang, Zhengxie Wu, Chunhua Xu, Dongyuan Xu, Zhengyong Jin
Apoptosis is an important process to eliminate damaged cells to maintain the normal physiological functioning of the body. It is mainly caused by the imbalance of anti- and pro-apoptotic proteins, among which the Bcl-2 protein family plays an important role.27,28 It has recently been reported that apoptosis is an important pathophysiological factor leading to lung injury29,30 and that the inhibition of apoptotic signaling pathways is essential to relieve lung injury. Previous studies have shown that IGF-1 has anti-apoptotic properties,18 and that in ischemic diseases, IGF-1 can inhibit cell apoptosis and protect against reperfusion injury.31 IGF-1 also protects against diabetic cardiomyopathy by inhibiting cardiomyocyte apoptosis.18 In addition, in Parkinson’s disease, IGF-1 protects SH-SY5Y cells through a cascade that inhibits apoptosis.32 In our study, IGF-1 treatment could significantly down-regulate the expression of the pro-apoptotic Bax and Caspase-3, which indicates that IGF-1 can inhibit hyperoxia-induced lung tissue apoptosis.