Advanced searches left 3/3

Apoptosis - Springer Nature

Summarized by Plex Scholar
Last Updated: 25 July 2022

* If you want to update the article please login/register

Mitochondria-Mediated Moderation of Apoptosis by EGCG in Cytotoxic Neuronal Cells Induced by Lead (Pb) and Amyloid Peptides

Lead exposure has been linked to Alzheimer's disease progression in Alzheimer's disease in the United States, according to scientific, epigenetic, and epidemiological studies on lead toxicity. The experimental groups were created initially by treating Pb and APs individually and in various combinations, as well as the presence of EGCG, and are compared to the Pb and AP groups with no EGCG exposure. When compared to the group without EGCG therapy, the EGCG-treated group has seen a significant rise in antioxidant marker expression levels and a decrease in oxidative stress marker levels, as shown by our analysis. In comparison to the group without EGCG therapy, a significant decrease in expression levels of VDAC and cytochrome c was seen in the EGCG-treated group, as well as the group without EGCG treatment.

Source link: https://doi.org/10.1007/s12011-021-02959-w


RPL38 knockdown inhibits the inflammation and apoptosis in chondrocytes through regulating METTL3-mediated SOCS2 m6A modification in osteoarthritis

Background Ribosomal protein L38 was found to be upregulated in osteoarthritic peripheral blood mononuclear cells, but the role in osteoarthritis progression has yet to be established. Methods By Western blotting, the protein levels of RPL38 and SOCS2 in cartilage tissue from OA patients and controls were discovered. Primary chondrocytes were stimulated by IL-1u03b2 to create an OA cell model, and RPL38 siRNA was transfected into chondrocytes to see the effects of RPL38's knockdown on cell viability, apoptosis, inflammatory factor secretion, and extracellular matrix degradation. Then, the mechanism by which RPL38 regulates SOCS2 expression and SOCS2-induced chondrocyte dysfunction was investigated. In addition, the effects of SOCS2 overexpression on IL-1-induced chondrocyte dysfunction and SOCS2 knockdown by siRPL38 were investigated. RPL38 directly interacted with METTL3 and inhibited SOCS2 expression by METTL3-mediated m6A conversion, which inhibited SOCS2 expression. In OA mice, a RPL38 knockdown reduced cartilage tissue damage and ECM degradation.

Source link: https://doi.org/10.1007/s00011-022-01579-x


Neuroprotective effects of 18β-glycyrrhetinic acid against bisphenol A-induced neurotoxicity in rats: involvement of neuronal apoptosis, endoplasmic reticulum stress and JAK1/STAT1 signaling pathway

BPA-induced neurotoxicity was expected to investigate the ameliorative effects of 18u03b2-glycerrhetinic acid on BPA-induced neurotoxicity. The IV-250 mg/kg BPA+ 100 mg/kg BPA+ 100 mg/kg BPA+ 100 mg/kg 18-u03b2-GA group, II-Control group, III-BPA company, III-BPA group, II-90 mg/kg BPA+ 50 mg/kg BPA+ 50 mg/kg 18u03b2-GA group, III-B2-GA company, I-Control group, I-Control corporation, III-B2GA corporation, 176 mg/b2-GA company, BPA-B2-GA group, 18u03b2-GA company, 18UG BPA+ 100 mg/kg BPA-BA, BPA+ 100 mg/kg BPA-B2-GA company, III-B2-GA company, III-GA company, III-BA, and BPA+ 50 mg/kg BPA, 18B2-GA company, b2-GA company, III-B2-GA company, and III-BA plant, BPA group, BPA+ 50 mg/kg BPA, and BPA intoxication was linked to elevated MDA levels, but reduced GSH concentration, superoxide dismutase, and catalase were all correlated with increased BPA intoxication, while catalase's activity was reduced. BPA also caused endoplasmic reticulum stress by raising mRNA transcript levels of PERK, IRE1, ATF-6, and GRP78. In addition, it was discovered that the BPA administration activated JAK1/STAT1 signaling pathway and levels of TNF-u03b1, NF-u03b1, p38 MAPK, and JNK in the brain. Overall, the findings of this research show that brain injury caused by BPA poisoning could be reduced by 18-u03b2-GA administration.

Source link: https://doi.org/10.1007/s11011-022-01027-z


High glucose-induced ROS-accumulation in embryo-larval stages of zebrafish leads to mitochondria-mediated apoptosis

zebrafish can mimic human diabetes' normal metabolic processes as an excellent model animal. In this research, we developed a diabetic zebrafish larvae model. We hope that this report will provide valuable reference information for type 2 juvenile diabetes care.

Source link: https://doi.org/10.1007/s10495-022-01731-2


Enhancing or inhibiting apoptosis? The effects of ucMSC-Ex in the treatment of different degrees of traumatic pancreatitis

The animal models of traumatic pancreatitis were developed to determine the specific mechanisms by which umbilical cord mesenchymal stem cell-derived exosomes produce therapeutic effects. Sixty four rats were randomly divided into eight groups, including TP groups with three distinct degrees and specific groups with ucMSC-Ex treated. The pancreatic histopathological score and serum amylase and lipase levels gradually increased in various degrees of TP and treatment regimens, which were all significantly reduced. In TUNEL results, the apoptosis index gradually increased in each TP group and dramatically decreased in the treatment group. Both WB and RT-qPCR followed the same pattern, with bax and caspase-3 gradually increasing, and bcl-2 gradually decreased in TP groups. The expression of bax and caspase-3 in comparison to TP groups was lower in the treatment group, but bcl-2 expression was higher.

Source link: https://doi.org/10.1007/s10495-022-01732-1


Lysophosphatidylcholine Acyltransferase 1 Deficiency Promotes Pulmonary Emphysema via Apoptosis of Alveolar Epithelial Cells

Inhalation of cigarette smoke is the third leading cause of death worldwide, and chronic obstructive pulmonary disease is mainly related to inhalation of cigarette smoke. Lysophosphatidylcholine acyltransferase 1 is an enzyme that catalyzes the biosynthesis of surfactant lipids and is present in type 2 alveolar epithelial cells. We analyzed an elastase-induced emphysema model using Lpcat1 knockout mice to determine the role of LPCAT1 in COPD's pathology. We then analyzed the effects of cigarette smoking on primary human type 2 epithelial cells, finding that cigarette smoke extract downregulated the expression of Lpcat1 genes. Taking together, cigarette smokeu2013-induced downregulation of LPCAT1 can promote the exacerbation of pulmonary emphysema by raising the susceptibility of alveolar epithelial cells to apoptosis, thereby suggesting that Lp1 is a novel therapeutic target for irreversible emphysema.

Source link: https://doi.org/10.1007/s10753-022-01659-4


Gold nanoparticles induce apoptosis in HCT-116 colon cancer cell line

Introduction This research was conducted in the hope of determining the apoptotic and anti-cancer effects of gold nanoparticles on apoptosis in HCT-116 colon cancer cells. Bcl-2, P53 genes, and a significant decrease in the expression of Bcl-2, CCNB1 genes at concentrations of 25 and 50 g/ml during 48 hours of incubation increased expression in Bax, P53 genes, as well as a significant decrease in Bcl-2, CCNB1 genes during 48 hours of incubation, according to control cells. During 48 h of incubation, AuNPs caused apoptosis at the half-maximal inhibitory concentration in the HCT-116 tumor cells, according to the authors.

Source link: https://doi.org/10.1007/s11033-022-07616-6


Sesquiterpene from Polygonum barbatum disrupts mitochondrial membrane potential to induce apoptosis and inhibits metastasis by downregulating matrix metalloproteinase and osteopontin in NCI-H460 cells

About 18% of cancer-associated mortalities worldwide, lung cancer accounts for 18% of cancer-related mortalities. Non-small cell lung cancer is the most common among the subtypes. Therefore, this study was intended to investigate the underlying molecular mechanism of apoptosis and metastasis against NCI-H460 cells, based on these findings. The molecular mechanism of compound 3 inducing apoptosis and inhibiting metastasis was discovered by testing mitochondrial membrane potential, DNA fragmentation, clonogenic assay, invasion assay, and expression of apoptotic and metastatic markers. Cell proliferation and cell proliferation were greatly reduced by cell proliferation and triggered apoptosis by the mitochondrial pathway, i. e. , by disrupting mitochondrial membrane potential. Moreover, compound 3 reduced the invasive nature of NCI-H460 cells evinced in Boyden chamber invasion assay and downregulating the expression of metastatic markers, i. e. , matrix metalloproteinase 2/9, and VEGF, respectively. Ostepontin was also found to be blocked by negatively regulating its expression, a key protein in cancer prevention.

Source link: https://doi.org/10.1007/s00210-022-02256-w


Melatonin induces apoptosis and cell cycle arrest in cervical cancer cells via inhibition of NF-κB pathway

Cervical cancer is the most common cancer in females. We investigated the dose-dependent anti-tumor response of melatonin against cervical cancer cell lines in HeLa and SiHa. respectively, the HeLa and SiHa cells are arrested by melatonin arrests during sub-G1 and G1 phases. Melatonin downregulated the expression of pro-inflammatory transcription factor, NF-u03baB, and the expression of COX-2 protein, a key mediator in cell proliferation, according to a Western blot report, a key factor in cell proliferation. Overall, the results show that melatonin showed strong anti-canceral activity against human cervical cancer cell line progression, despite inhibition of the NF-u03baB signaling pathway.

Source link: https://doi.org/10.1007/s10787-022-00964-6


ML323, a USP1 inhibitor triggers cell cycle arrest, apoptosis and autophagy in esophageal squamous cell carcinoma cells

Esophageal squamous cell carcinoma is a common digestive cancer with high mortality due to late diagnosis and drug resistance. ML323 inhibited esophageal cancer cell viability and colony formation, according to the researchers. In contrast, ML323 blocked cells at G0/G1 phase concomitant with reduced protein content of c-Myc, cyclin D1, CDK4, and CDK6. DNA damage and active p53 were both related to DNA damage during ML323 therapy, which also resulted in DNA destruction and active p53. These results showed that the USP1 inhibitor could be used as a cost-effective anti-ESCC treatment.

Source link: https://doi.org/10.1007/s10495-022-01736-x

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions