1Department of Pharmacy, Nootan Pharmacy College, Sankalchand Patel University, Visnagar - 384315, Gujarat, India
2Department of Pharmacy, H. R. Patel Institute of Pharmaceutical Education and Research, Karwand Naka, Shirpur - 425405, Maharashtra, India
3Department of Pharmacy, Manjushree Institute of Pharmacy, Pethapur-Mahudi Road, Piplaj, Gandhinagar - 382610, India
4Department of Pharmacy, Parul Institute of Pharmacy & Research, Parul University, Vadodara - 391760, Gujarat, India
*Corresponding Author Email: shaktipalpatil@yahoo.com ORCID: https://orcid.org/0000-0003-0400-2022
Received: 12th Dec, 2025; Revised: 12th Feb 2026; Accepted: 13th Feb, 2026; Available Online: 10th March, 2026
Cognitive impairment progressively manifests in neurodegenerative diseases such as aging, moderate cognitive impairment, Alzheimer's disease, perioperative neurocognitive disorders, and stroke, imposing a substantial socioeconomic burden. This model demonstrates that cholinergic agonist, antioxidant, and anti-neuroinflammatory therapies yield beneficial outcomes. Pinoresinol diglucoside (PDG) exhibits numerous pharmacological actions. Nonetheless, there is a lack of evidence on the efficacy of PDG in ameliorating cognitive impairment induced by lipopolysaccharide (LPS). Consequently, we assessed its efficacy in mitigating cognitive impairment induced by LPS at a dosage of 1 mg/kg administered intraperitoneally in Wistar rats. To evaluate learning and memory performance, the Y-maze paradigm was employed. Oxidative stress was assessed by measuring the activities of superoxide dismutase (SOD) and catalase (CAT), along with the level of malondialdehyde (MDA), to determine their role in ameliorating cognitive decline. In addition, cholinergic function was examined through choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) levels, while neuroinflammatory status was determined by estimating interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) concentrations. PDG administration considerably improved behavioral performance in the Y-maze test. In addition, PDG modulated oxidative stress markers, as evidenced by changes in SOD, CAT, and MDA levels, and improved cholinergic function through regulation of AChE and ChAT activity. Furthermore, the levels of pro-inflammatory cytokines, including IL-6, TNF-α, and IL-1β, were significantly altered following treatment. Overall, these findings suggest that PDG exerts a protective effect against LPS-induced cognitive dysfunction.
Keywords: Lipopolysaccharide, Cognitive impairment, Pinoresinol Diglucoside, Oxidative stress, Pro-inflammatory cytokines
How to cite this article: Patil S, Shah U, Chaudhary H, Das Mandal S. Neuroprotective Effects of Pinoresinol Diglucoside in Lipopolysaccharide-Induced Cognitive Impairment: Behavioral, Biochemical and Molecular Evidences. Int J Drug Deliv Technol. 2026;16(3): 727. DOI: 10.25258/ijddt.16.3.80
Source of support: Nil.
Conflict of interest: None