Goji Berry as a Therapeutic Candidate in Age-associated Pulmonary Fibrosis: Insights into Collagen Regulation and Fibrotic Mechanisms

• Published in: Journal of Advances in Medical and Pharmaceutical Sciences Vol. 27; no. 7; pp. 59 - 68
• Main Authors: Bernadi, Joshua, Sumadi, I Wayan Juli
• Format: Journal Article
• Language: English
• Published: Science Domain International 21.07.2025
• Subjects: Computer Science; Medical Imaging
• ISSN: 2394-1111; 2394-1111
• DOI: 10.9734/jamps/2025/v27i7799

Introduction: Pulmonary fibrosis (PF) is a progressive lung disorder marked by excessive collagen accumulation and tissue remodeling, commonly associated with aging and oxidative stress. Goji berry (Lycium barbarum), a natural source of bioactive compounds such as Lycium barbarum polysaccharides (LBP), has demonstrated potential in mitigating oxidative lung damage and fibrotic changes due to its potent antioxidant and anti-inflammatory properties. This narrative review examines the molecular mechanisms through which Goji berry may help regulate oxidative stress, inflammation, and fibrosis in pulmonary tissues. Methods: A narrative literature review was conducted by systematically searching databases including Google Scholar, PubMed, ScienceDirect, and SpringerLink for studies published between 2004 and 2024. Eligible studies were selected based on predefined criteria, focusing on in vivo animal models evaluating the effects of Goji berry or LBP on pulmonary oxidative injury, inflammation, and fibrosis. Results and Discussion: Three key studies were analyzed. In aged mice, LBP (200–400 mg/kg/day) enhanced lung antioxidant enzyme levels (e.g., SOD, GPx) and significantly reduced markers of oxidative damage (e.g., MDA). In exercise-induced oxidative models, LBP (up to 300 mg/kg/day) improved antioxidant enzyme activity and lowered malondialdehyde (MDA), a marker of lipid peroxidation. Most notably, in a cigarette smoke-induced lung injury model, LBP (100–200 mg/kg/day) reduced TNF-α, IL-6, and IL-8, inhibited NF-κB signaling, and improved lung histology, demonstrating its potential to counteract both oxidative stress and inflammation. Across studies, Goji berry’s polysaccharides consistently demonstrated antioxidant, anti-inflammatory, and collagen-modulating effects that mitigated pulmonary fibrotic changes. Additionally, Goji berry's ability to reduce TGF-β and modulate fibrogenic signaling pathways offers a potential alternative or complementary strategy to current therapies like pirfenidone and nintedanib, which primarily target fibroblast activity but do not address the underlying oxidative damage. Conclusion: Goji berry, through its bioactive compound LBP, presents a promising natural therapeutic agent for managing pulmonary fibrosis. Its capacity to modulate oxidative stress, inflammation, and collagen deposition highlights its potential in reducing lung damage caused by aging or environmental exposure. However, further clinical validation and exploration into its synergistic effects with current therapies are warranted to establish its role in fibrosis treatment and its broader applicability in lung health. Future research should focus on large-scale clinical trials, optimizing dosing regimens, and assessing long-term safety and efficacy in human populations.