Targeting autophagy and UPR in NAFLD-induced renal injury: The role of Chlorella vulgaris and Lactobacillus casei.

Atefeh Raoofat, Morteza Jafarinia, Sanaz Dastghaib

J Nutr Biochem

May 7, 2026

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Abstract

Nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as a contributor to renal injury through mechanisms involving oxidative stress, inflammation, and cellular stress pathways. This study aimed to evaluate the protective effects of Chlorella vulgaris (CV), Lactobacillus casei (LBC), and their combination on NAFLD-induced renal damage by focusing on UPR, autophagy pathways in mice. NAFLD was induced in male C57BL/6 mice using a high-fat diet (HFD). Animals were divided into Control group, N.S group (HFD for 8 weeks+normal saline), CV group (HFD+CV), LBC group (HFD+LBC), and LBC+CV group (HFD+both LBC and CV). Molecular assessments included real-time PCR for UPR, autophagy (Beclin-1, LC3-IIβ, and p62), apoptosis (BAX, Bcl-2, and Caspase-3), and inflammation/oxidative stress markers (IL-6, NF-κB, and NRF-2). Biochemical parameters (ALT, AST, BUN, creatinine, uric acid, MDA, TAC, SOD, GPX, and Catalase) were measured. Histopathological evaluations were also conducted. NAFLD markedly impaired UPR signaling, inhibited autophagy, augmented apoptosis, and heightened inflammatory and oxidative stress markers in renal tissue. The administration of CV and LBC, especially in combination, rectified these molecular modifications. Antioxidant enzyme levels increased biochemically, but MDA levels diminished. Histologically, renal impairment, characterized by tubular dilation and glomerular injury, was significantly mitigated. Serum indicators of hepatic and renal impairment also showed improvement with treatment. CV and LBC confer renoprotective effects in NAFLD through multitarget mechanisms involving ER stress modulation, autophagy restoration, antiapoptotic action, and redox/inflammatory balance. These findings support their potential as complementary therapies for NAFLD-related kidney injury.