China
Africa
Explore chapters and articles related to this topic
Bone Regeneration Effect of Cassia occidentalis Linn. Extract and Its Isolated Compounds
Published in Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay, Phytochemistry of Plants of Genus Cassia, 2021
Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay
The anti-oxidant effect of kaempferol in osteoblasts has been studied. 2-Deoxy-D-ribose (dRib) is a sugar with a high reducing capacity and induces oxidative stress and kaempferol mitigates dRib-induced oxidative stress in MC3T3-E1 cells by reducing malondialdehyde content (Suh et al., 2009). Kaempferol is also known to activate both ERα- and ERβ transactivation and promote the expression of osteogenic genes (Guo et al., 2012; Tang et al., 2008). In MC3T3-E1 cells, induction of differentiation by kaempferol was accompanied by autophagy assessed by the expression of beclin-1, sequestosome-1, and conversion of LC3-II to LC3-I (Kim et al., 2016). Kaempferol also protects osteoblasts against dexamethasone-induced apoptosis through the activation of the ERK pathway (Adhikary et al., 2018). Together the data suggest that kaempferol promotes osteogenic differentiation, protects against oxidative stress, and drug-induced apoptosis. The signaling mechanisms are varied including ER, BMP, mTOR and autophagy pathways.
Role of Vitamin D and Antioxidant Functional Foods in the Prevention and Treatment of Alzheimer’s Disease Pathology
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Mediators of apoptosis involved in AD disease include c-jun (the protein encoded by the JUN gene that forms the AP-1 early response transcription factor), BCL2 (apoptosis regulator B-cell lymphoma 2 protein), and BCL-xL (B-cell lymphoma-extra-large, apoptosis-related transmembrane molecule in the mitochondria). A decrease in BLC2 is observed in NFT and an increase in Bax (apoptosis regulator) is observed in neurons of some microglia in AD brains. Some of the caspases involved include caspases 3/6 and 9 which can be associated with misfolded tau. Even though apoptosis is a contributor to the cell death observed in AD, it is not confirmed that it is responsible for all death observed with this disease. Apoptosis may not be significantly increased in AD animal disease models. In humans, necrosis is also an important contributor to AD cell death. One mechanism thought to be relevant in neuronal loss synaptic loss is nonapoptotic sublethal caspase activation in the dendrite’s axons. Inhibition of apoptosis protein and proteasome activity may have a role in leading the cell fat into a nonapoptotic pathway. Beclin-1 (protein encoded by the BECN1 gene) expression is decreased in human brains during aging and reduces beta-amyloid pathology in APP mice.
Lung cancer inhalation therapeutics
Published in Anthony J. Hickey, Heidi M. Mansour, Inhalation Aerosols, 2019
Several investigators have successfully delivered genes by inhalation using these nonviral carriers. Inhalation of p53 tumor suppressor gene in lipoplexes containing polylysine and protamine reduced lung metastasis in a murine model of malignant melanoma (167). Likewise, upregulation of beclin-1, a tumor suppressor gene involved in autophagy, sensitized tumor cells to radiation therapy (168). Another approach involves transfection of tumors with a gene that codes for a specific enzyme that transforms a benign drug into a toxic metabolite that causes cell death (“suicide gene”). For example, transduction of herpes simplex virus 1 thymidine kinase (HSVtk) gene makes cells susceptible to ganciclovir, a nucleoside analogue, which is normally poorly metabolized by mammalian cells. HSVtk converts ganciclovir to a metabolite that causes cell death by interfering with DNA replication. Clinical trials have employed an adenoviral vector to transduce HSVtk by intratumoral injection into mesothelioma with partial success (169). Inhalation of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) tumor suppressor gene with glycosylated conjugated PEI resulted in expression of a functional PTEN protein in the lung with reduced phosphorylation of its target protein and apoptosis in transduced lung cells (170).
Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy
Published in Renal Failure, 2023
Zhongdi Liu, Yifan Chen, Zhe Du, Fengxue Zhu, Wei Huang
LC3 is a marker of autophagy, when autophagy occurs, cytoplasmic LC3 (LC3-I) will enzymically remove a small fragment of polypeptide and transform into membrane type (LC3-II). Therefore, the size of LC3-II/I ratio can estimate the level of autophagy. Beclin 1 is involved in the formation of autophagosome membrane and plays an important role in regulating apoptosis and autophagy [38]. A better understanding of the crosstalk between autophagy and the inflammatory response will contribute to the design of more effective approaches to treat AKI after LIR [39]. For example, it has been reported that exonuclear HMGB1 can directly or indirectly activate cytoplasmic Beclin1. It has been shown in tumor cells that ROS promote the transport of HMGB1 from the nucleus to the cytoplasm, while cytoplasmic HMGB1 interacts with Beclin-1, which, in turn, is released from the Beclin-1/Bcl-2 complex and induces autophagy [38,40].
Autophagy-dependent ferroptosis is involved in the development of endometriosis
Published in Gynecological Endocrinology, 2023
Hui Li, Huadi Yang, Shenyi Lu, Xinyan Wang, Xinhe Shi, Peiyu Mao
Autophagy is a cellular degradation process that removes and recycles damaged proteins and organelles through the lysosomal machinery. Initiated by the formation of a phagophore, a double-membrane structure, autophagy is mediated by various Atg proteins that control the expansion of the phagophore, resulting in an autophagosome. Several Atgs are associated with autophagy, among which LC3 and Beclin1 are significant factors [7]. LC3, a gene homologous to the Atg8 autophagy-related gene in yeast, is a unique marker of autophagosomes, and its expression level directly signifies the degree of autophagy [8]. Beclin1 also referred to as BECN 1, is an autophagy-specific gene, a tumor suppressor gene related to autophagy, and a direct autophagy regulator in mammals [9]. The autophagosome then merges with a lysosome, leading to the degradation and recycling of its content [10,11]. This process plays a pivotal role in maintaining cellular homeostasis. Dysregulation of autophagy, as has been suggested in the context of EMS, may promote the survival and proliferation of ectopic endometrial cells [3]. EMS exhibits numerous tumor disease traits, including metastasis, implantation, and recurrence [12,13]. Various studies have reported a link between autophagy and several malignant tumors. For instance, a decrease in autophagy activity has been associated with the onset and progression of various cancers, including pancreatic, breast, cervical squamous cell, colon, and ovarian cancer, indicating a strong correlation between the abnormal expression of autophagy-related genes and tumor development [14,15].
The role of autophagy in acute myeloid leukemia development
Published in Expert Review of Anticancer Therapy, 2023
Martyna Bednarczyk, Karolina Kociszewska, Olga Grosicka, Sebastian Grosicki
Proteins from the Bcl-2 and Bcl-XL group, involved in apoptosis, also participate in autophagy by acting as its’ inhibitors. In some cell types of these proteins bind to Beclin 1, lowering its affinity for PI3K III. The role of these proteins in autophagy is related to the fact that the Bcl-2/Bcl-XL-Beclin 1-PI3K complex has a lower kinase activity than the complex without the attached Bcl-2 or Bcl-XL proteins. Interactions between Beclin1 and the above-mentioned proteins are regulated by their phosphorylation status. The DAPK-1 kinase (Death-associated protein kinase 1) phosphorylates Beclin1, while the JNK1 kinase (c-Jun N-terminal kinases) phosphorylates the Bcl-2 protein. These proteins then become disconnected, inducing autophagy. In addition, the phosphorylated protein Bcl-2 combines with the pro-apoptotic protein Bax, inhibiting apoptosis [23]. Figure 2 shows involved of autophagy in cancer development.