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Biology subjects

Perumal, D.

Publications and source records attributed to Perumal, D..

3 recordsLinked to original sources

Combined statin probiotic treatment mitigates atherogenic dyslipidemia fueling NAFLD in high-cholesterol-diet fed rats

Background: Chronic hypercholesterolemia accelerates metabolic dysregulation, systemic oxidative stress, and endothelial dysfunction, driving the initiation and progression of atherogenesis. Although statins like Atorvastatin (AS) represent the clinical cornerstone of lipid lowering therapy, long term high dose use is often constrained by adverse side effects. Probiotic interventions targeting the gut heart axis, such as Bifidobacterium longum (B), offer a promising therapeutic strategy to enhance lipid homeostasis and reduce vascular inflammation. Methods: Male rats were fed a High Cholesterol Diet (HCD) for 120 days to establish hypercholesterolemia, dyslipidemia, and systemic vascular pathology. Experimental groups were administered AS monotherapy, B. longum monotherapy, or their dual combination (AS + B) daily from day 90 to 120. Redox dynamics (GSH, MDA, GSH/MDA ratio), functional HDL associated proteins (PON1, APOA1), circulating oxidized LDL (oxLDL), inflammatory cytokines (CRP, TNF alpha;, IL 6, IL 8), and all adhesion molecules (ICAM 1, VCAM 1) were quantified, alongside histopathological evaluation of hepatic and aortic tissue microarchitecture. Results: High cholesterol diet feeding induced severe dyslipidemia, vascular remodeling, lipid peroxidation, and endothelial inflammation in rats. Monotherapy with Atorvastatin (AS) or Bifidobacterium longum (B) significantly reversed metabolic impairment (p<0.001), while dual AS + B therapy achieved maximum efficacy (p<0.01 vs. AS alone) in restoring hepatic and aortic microarchitecture. Mechanistically, combination treatment blunted oxidative stress by minimizing malondialdehyde and upregulating Paraoxonase 1 and Apolipoprotein A1 (p<0.01), which markedly suppressed low density lipoprotein oxidation (p<0.001). Furthermore, dual therapy yielded the maximum downregulation of pro inflammatory cytokines (C reactive protein, tumor necrosis factor alpha;, interleukin 6, interleukin 8) and adhesion molecules (ICAM1,VCAM1); p<0.001), demonstrating potent anti inflammatory effect against diet induced atherogenesis. Conclusion: Co administration of Atorvastatin and Bifidobacterium longum demonstrates multi targeted therapeutic synergy by effectively restoring HDL functional capacity, attenuating vascular endothelial inflammation, and mitigating hypercholesterolemia simultaneously, this dual pharmacological probiotic strategy provides a robust, novel intervention against diet induced atherogenesis. Keywords: Hypercholesterolemia, Atorvastatin, Bifidobacterium longum, Lipid Peroxidation, Endothelial Dysfunction, Vascular Inflammation

biochemistry↗

Temporal changes in miR-23a-5p levels in subclinical atherosclerosis: A Potential biomarker.

A high-cholesterol diet (HCD) is a well-established contributor to oxidative stress, inflammation, and atherogenesis, yet the temporal progression of these pathological changes and the regulatory role of circulating microRNAs (miRNAs) remain incompletely understood. In this study, we investigated the effects of prolonged HCD exposure to rats on lipid metabolism, oxidative stress, inflammation, endothelial dysfunction, and miRNA expression in a rat model. Male Wistar rats were fed either a standard diet or HCD for 30, 60, 90, or 120 days. Biochemical analyses revealed a progressive dyslipidemic profile characterized by elevated total cholesterol, triglycerides, LDL, VLDL, and atherogenic index, alongside a significant reduction in HDL. Lipid peroxidation levels increased markedly with HCD duration, while antioxidant markers PON1 and ApoA1 were significantly reduced and oxLDL levels were elevated. Inflammatory cytokines (CRP, TNF-, IL-6, IL-8) and VCAM-1 were significantly increased, indicating systemic inflammation and endothelial activation. Notably, miR-23a-5p and miR-15b-5p were elevated in the serum of HCD-fed rats, with miR-23a-5p peaking at day 120. Correlation analyses revealed that miR-23a-5p expression positively correlated with oxLDL and inversely with ApoA1 and PON1 levels, suggesting its involvement in oxidative and lipoprotein dysregulation. These findings demonstrate that prolonged HCD induces a coordinated cascade of oxidative, inflammatory, and lipoprotein alterations, with miR-23a-5p emerging as promising biomarkers and potential regulators of redox and lipid homeostasis in atherogenesis.

molecular biology↗

Pathognomonic and epistatic genetic alterations in B-cell non-Hodgkin lymphoma

B-cell non-Hodgkins lymphoma (B-NHL) encompasses multiple clinically and phenotypically distinct subtypes of malignancy with unique molecular etiologies. Common subtypes of B-NHL such as diffuse large B-cell lymphoma (DLBCL) have been comprehensively interrogated at the genomic level. But rarer subtypes such as mantle cell lymphoma (MCL) remain sparsely characterized. Furthermore, multiple B-NHL subtypes have thus far not been comprehensively compared using the same methodology to identify conserved or subtype-specific patterns of genomic alterations. Here, we employed a large targeted hybrid-capture sequencing approach encompassing 380 genes to interrogate the genomic landscapes of 685 B-NHL tumors at high depth; including DLBCL, MCL, follicular lymphoma (FL), and Burkitt lymphoma (BL). We identified conserved hallmarks of B-NHL that were deregulated in the majority of tumor from each subtype, including the frequent genetic deregulation of the ubiquitin proteasome system (UPS). In addition, we identified subtype-specific patterns of genetic alterations, including clusters of co-occurring mutations and DNA copy number alterations. The cumulative burden of mutations within a single cluster were more discriminatory of B-NHL subtypes than individual mutations, implicating likely patterns of genetic cooperation that contribute to disease etiology. We therefore provide the first cross-sectional analysis of mutations and DNA copy number alterations across major B-NHL subtypes and a framework of co-occurring genetic alterations that deregulate genetic hallmarks and likely cooperate in lymphomagenesis.

genomics↗