Last update 01 Nov 2024

Malondialdehyde

Last update 01 Nov 2024

Basic Info

Synonyms-

Introduction-

Drugs associated with Malondialdehyde

Malondialdehyde inhibitors(Nanjing Medical University)

Target

Malondialdehyde

Mechanism

Malondialdehyde inhibitors

Active Org.

Nanjing Medical University

Originator Org.

Nanjing Medical University

Active Indication

Asthma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Malondialdehyde

CTRI/2024/09/073683 / Not yet recruitingPhase 2IIT

Evaluation of the efficacy of a novel Proanthocyanidin gel as an adjunct to minimally invasive non surgical therapy (MINST) in periodontitis. - NIL

Start Date30 Sep 2024

Sponsor / Collaborator-

100 Clinical Results associated with Malondialdehyde

100 Translational Medicine associated with Malondialdehyde

0 Patents (Medical) associated with Malondialdehyde

3,042

Literatures (Medical) associated with Malondialdehyde

01 Jan 2025·Journal of Ethnopharmacology

Anti-fatigue effect of an enzymatically derived deer velvet extract through muscle damage recovery and improvement of antioxidant levels

Article

Author: Jeong, Jeongho ; Park, Cho I ; Park, Hyun-Je ; Seo, Jae Won ; Song, Aeri ; Kim, Junghyun ; Park, Kun Hee ; Kim, Hye Lim ; Cha, Joo Young

ETHNOPHARMACOLOGICAL RELEVANCEDeer velvet (DV) has been extensively used in traditional Oriental medicine to treat various diseases. Its pharmacological spectrum encompasses tonicity, longitudinal bone growth of adolescence, blood retention, hemopoiesis facilitation, enhancement of organ function, physical function improvement, and augmentation of physical vitality. Among its myriad effects, DV notably exhibits anti-fatigue properties; however, its specific mode of action is yet to be fully elucidated.AIM OF THE STUDYThis study was undertaken to investigate the anti-fatigue and exercise performance-enhancing effects of YC-1101(HENKIV®), an enzymatically derived DV extract, in C2C12 cell lines and forced swimming mouse models.MATERIALS AND METHODSThe effect of YC-1101 on increasing cell growth and lowering lactate dehydrogenase (LDH) activity was assessed in C2C12. The antioxidative effects of YC-1101 and its mechanistic underpinnings were also evaluated in C2C12 cells. Moreover, mice were subjected to an exhaustive swimming test subsequent to 3 weeks of YC-1101 extract administration. Fatigue-associated biochemical parameters, such as LDH activity and lactate, superoxide dismutase, glutathione peroxidase, and malondialdehyde levels, were measured in serum and muscle tissues.RESULTSYC-1101 significantly promoted myoblast growth and reduced LDH activity, indicative of a cell-proliferative effect. Notably, free radical scavenging assays and analysis of reactive oxygen species production and antioxidant-related mRNA expression corroborated the significant involvement of YC-1101 in antioxidation, an important mechanism in anti-fatigue processes. Furthermore, animal experiments demonstrated prolonged swimming endurance and inhibition of muscle LDH accumulation in forced swimming mouse models. Serum biochemical analysis further revealed significant modulation of the expression of anti-fatigue-related biomarkers. Various bioactive low-molecular-weight DV peptides were enriched in YC-1101 compared to YHC-BE-2038 (a DV extract without enzymatic digestion). The anti-fatigue effect of YC-1101 was significantly stronger than that of YHC-BE-2038.CONCLUSIONSThese findings suggest the potential of YC-1101 as a nutraceutical adjunct in ameliorating fatigue, concurrently facilitating muscle damage recovery, and exerting antioxidant effects via the nuclear factor E2-related factor 2-Kelch-like ECH-associated protein-1 pathway. It can be assumed that the complex action of low-molecular-weight DV peptides produced during the enzymatic degradation process was effective, and the further research is needed.

31 Dec 2024·Virulence

Porcine reproductive and respiratory syndrome virus infects the reproductive system of male piglets and impairs development of the blood–testis barrier

Article

Author: Xu, Zhiwen ; Deng, Lishuang ; Zeng, Xiu ; Zhou, Yuancheng ; Huang, Bingzhou ; Lai, Siyuan ; Ai, Yanru ; Zhu, Ling ; Huang, Jianbo ; You, Dong ; Ge, Liangpeng ; Li, Fengqin ; Xu, Tong

Porcine reproductive and respiratory syndrome virus (PRRSV) causes a highly contagious disease that threatens the global swine industry. Recent studies have focused on the damage that PRRSV causes to the reproductive system of male pigs, although pathological research is lacking. Therefore, we examined the pathogenic mechanisms in male piglets infected with PRRSV. Gross and histopathological changes indicated that PRRSV affected the entire reproductive system, as confirmed via immunohistochemical analysis. PRRSV infected Sertoli cells and spermatogonia. To test the new hypothesis that PRRSV infection in piglets impairs blood - testis barrier (BTB) development, we investigated the pathology of PRRSV damage in the BTB. PRRSV infection significantly decreased the quantity and proliferative capacity of Sertoli cells constituting the BTB. Zonula occludens-1 and β-catenin were downregulated in cell - cell junctions. Transcriptome analysis revealed that several crucial genes and signalling pathways involved in the growth and development of Leydig cells, Sertoli cells, and tight junctions in the testes were downregulated. Apoptosis, necroptosis, inflammatory, and oxidative stress-related pathways were activated, whereas hormone secretion-related pathways were inhibited. Many Sertoli cells and spermatogonia underwent apoptosis during early differentiation. Infected piglets exhibited disrupted androgen secretion, leading to significantly reduced testosterone and anti-Müllerian hormone levels. A cytokine storm occurred, notably upregulating cytokines such as tumour necrosis factor-α and interleukin-6. Markers of oxidative-stress damage (i.e. H₂O₂, malondialdehyde, and glutathione) were upregulated, whereas antioxidant-enzyme activities (i.e. superoxide dismutase, total antioxidant capacity, and catalase) were downregulated. Our results demonstrated that PRRSV infected multiple organs in the male reproductive system, which impaired growth in the BTB.

31 Dec 2024·Future Science OA

Effect of pentoxifylline on endothelial dysfunction, oxidative stress and inflammatory markers in STEMI patients

Article

Author: Ahmed, Marwa Adel ; Saleh, Mohamed Ayman ; Sabri, Nagwa Ali ; Farouk, Mohamed Moustafa ; Saeed, Asmaa

Aim: ST-elevation myocardial infarction (STEMI) patients suffer higher mortality and adverse outcomes linked to endothelial dysfunction (ED). Methods: 43 patients were randomized to pentoxifylline (PTX) 400 mg thrice daily (n = 22) or placebo (n = 21). Soluble vascular cell adhesion molecule-1, malondialdehyde, interleukin-1 (IL-1), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-α (TNF-α) were assessed at baseline and 2 months. Results: After 2 months, no significant difference was observed in markers' levels between the 2 groups. However, a within-group comparison revealed a statistically significant change in hs-CRP in the PTX group (10.057 (9.779–10.331) versus 9.721 (6.102–10.191)), p = 0.032. Conclusion: PTX for 2 months in STEMI patients was safe and well-tolerated but had no significant detectable effect on ED, oxidative stress or inflammatory markers. Clinical Trial Registration: NCT04367935 ( ClinicalTrials.gov )

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