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Ethnomedicinal Plants of North Eastern Himalayan Region of India to Combat Hypertension
Published in Amit Baran Sharangi, K. V. Peter, Medicinal Plants, 2023
Pintubala Kshetri, K. Tamreihao, Subhra Saikat Roy, Thangjam Surchandra Singh, Susheel Kumar Sharma, Meraj Alam Ansari
Andrographolide is the bioactive phytoconstituent isolated from various parts of Andrographis paniculata. It exhibits anti-HIV, anti-inflammatory, and antineoplastic properties (Chen et al., 2014; Jayakumar, 2013). Yoopan et al. (2007) studied the effects of three active diterpenoids viz., andrographolide (AP1), 14-deoxy-11, 12-didehydroandrographolide (AP3) and neoandrographolide on BP, vascular, and chronotropic responses by using conscious rats and their isolated Arotas as test model. They found that AP3 was most effective for inducing vasorelaxation and retarding heart rate and had a greater hypotensive effect in conscious rats than the AP1. Their result suggests that vascular muscle is the major site of hypotensive effect of AP3. Similarly, Mali et al. (2017) also showed that application of andrographolide loaded scleroglucan based formulation inhaler in rat increased lung deposition of andrographolide powder in lung and pulmonary antihypertensive activity.
Pathogenesis: Molecular mechanisms of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Anastasia E. Markatseli, Theodora E. Markatseli, Alexandros A. Drosos
RANKL binds to the osteoclast cell-surface receptor RANK. Subsequently, RANK is trimerized and recruits a member of the TNF receptor-associated factors (TRAFs) at specific sites within its cytoplasmic domain (167). These factors are TRAF 2, 5, and 6. The most basic factor for osteoclasts (precursors and mature) seems to be TRAF 6 (56,168). The signaling pathways that are activated after the binding of RANK with TRAF are as follows: Four pathways that induce the formation of osteoclasts: (a) inhibitor of NF-κB kinase (IKK)/NF-κB), (b) nuclear factor of activated T cells (NFATc1), (c) c-Jun N-terminal kinase (JNK)/activator protein-1 (AP-1), and (d) c-myc.Three pathways that mediate activation ([a] MKK6/p38/MITF and [b] Src) and survival of osteoclasts ([a] kinase pathway regulated by extracellular signal and [b] Src pathway) (169). Figure 2.2a summarizes the signal transduction pathways after RANK.
Structure and Function of the Urokinase-Type Plasminogen Activator Gene
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Yoshikuni Negamine, Janet S. Lee, Pierre-Alain Menoud, Rika Nanbu
It is obvious from the sequence comparison (see Figure 4) that the AP1 element in the PEA3/API site has the consensus sequence TGARGTCA and is different from the AP1 consensus sequence TGAGTCA71,72 by an additional purine base at the center of the symmetry. The significance of this deviation from the authentic AP1 sequence for u-PA gene regulation is not yet clear. We tested a u-PA gene construct in which the API-like sequence TGAGGTCAT was converted to an authentic AP1 TGAGTCA. This mutation enhanced TPA-mediated induction by twofold but had no significant effect on the induction by cytoskeletal reorganization or okadaic acid.53,66 Considering the developmental and tissue-specific regulation, it would be interesting to test this construct in transgenic mice.
Evaluation of JUN, FN1 and LAMB1 polymorphisms in pterygium in a Chinese Han population
Published in Ophthalmic Genetics, 2022
Xiying Wu, Shiqi Dong, Yuting Xu, Ge Zhu, Ming Yan
JUN is proto-oncogene located on chromosome 1p32-p31, a chromosomal region involved in both translocations and deletions in human malignancies. JUN protein is a major component of the activator protein-1 (AP-1) complex. There is evidence that AP-1 proteins control cell proliferation and death through their ability to regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21, p19, and p16 (25). Tong reported JUN and LAMB1 were down-regulated in pterygium, while FN1 was up-regulated (26); the result coincided with our research. According to Xu’s study, small interfering RNA-importin 13 (siRNA-IPO13) efficiently prevented nuclear translocation of JUN in pterygium epithelial cells, and IPO13 might play a role in the development of pterygium through modulation of keratin 17 and JUN (27). One hypothesis is that JUN may directly or indirectly affect the normal cell cycle, leading to the formation of pterygium.
DNA methyltransferase inhibitors increase NOD-like receptor activity and expression in a monocytic cell line
Published in Immunopharmacology and Immunotoxicology, 2022
Claire L. Feerick, Declan P. McKernan
NOD1 and NOD2 receptors transduce bacterial signals via similar pathways. Both recognize and bind specific components of the invading peptidoglycan (iE-DAP/TRI-DAP or MDP) via their LRR domains [10]. Active receptors subsequently recruit and bind the RIP2 adapter protein, via CARD-CARD interactions, which in turn is activated via auto-phosphorylation [11]. This initiates a cascade of ubiquitination and phosphorylation events leading to the liberation of the nuclear factor‐κB (NF‐κB) transcription factor from its inhibitor (IκBα) and activation of mitogen‐activating protein kinases (MAPKs) such as p38 and extracellular signal‐regulated kinase (ERK). These MAPKs are upstream promoters of the activator protein‐1 (AP1) transcription factor. NF‐κB and AP-1 transcription factors subsequently translocate to the nucleus to promote expression of pro‐inflammatory mediators including cytokines (e.g. TNF-α and IL-6) and chemokines (e.g. IL-8) [9,12].
Combination of tetrandrine and 3-n-butylphthalide protects against cerebral ischemia-reperfusion injury via ATF2/TLR4 pathway
Published in Immunopharmacology and Immunotoxicology, 2021
Cunfang Li, Aijun Chai, Yongchao Gao, Xuan Qi, Xuguang Zheng
ATF2 family is a member of is a member of AP1 transcription factor family. It forms with other AP1 members to modulate gene expression. ATF2, activated by stress stimuli, such as oxidative stress, hypoxia, inflammatory response, etc., enhances microglial inflammatory activation and neurodegeneration [30,31]. For instance, oxidative stress-induced activation of ATF2 promotes MMP9 transcription and astrocytic migration [32]. Activity deprivation cerebellar granule neurons (CGNs) enhances the binding of c-Jun:ATF2 heterodimers to the caspase-3 promoter and contribute to the apoptosis of CGNs [33]. In this study, ATF2 was upregulated after hypoxia. Overexpression of ATF2 antagonized the effects of TTD + NBP and induced the degeneration of neurons, manifested by the increase in apoptosis and inflammatory response, which was consistent with previous studies [30–33].