ArticleExperimental physiology2026
Impact of combined ginsenoside-MC1 and irisin on mitochondrial apoptosis in diabetic rats with hepatic reperfusion injury: Role of AMPK/JNK signalling.
Article in Experimental physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Hepatic ischaemia-reperfusion (IR) injury is a serious clinical issue, especially in patients with type 2 diabetes mellitus (T2DM). As mitochondria play a critical role in the regulation of IR-induced liver damage, mitochondria-targeted treatment is of the utmost significance for improving outcomes. The present study explored the mitoprotective role of combined ginsenoside-MC1 (GMC1) and irisin administration in diabetic rats with hepatic IR injury. T2DM was induced in male Sprague-Dawley rats with a high-fat diet and a low-dose streptozotocin. Following the induction of diabetes, hepatic IR injury was induced. Rats were pretreated with GMC1 and/or irisin for 28 days prior to IR injury. Liver function was evaluated by quantitation of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH). Histopathological changes were observed with haematoxylin-eosin staining. Apoptotic markers (Bax, Bcl-2, cleaved caspase-3) and signalling proteins (AMP-activated protein kinase (AMPK), c-Jun N-terminal kinase (JNK)) were examined by western blotting. Mitochondrial function was evaluated by measuring reactive oxygen species, membrane potential and ATP content. Oxidative stress markers, such as malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx), were also measured. Combined therapy lowered AST, ALT and LDH levels, and histopathological injury (P < 0.05). It restored mitochondrial function; upregulated Bcl-2 and phosphorylated AMPK expression; downregulated Bax, cleaved caspase-3 and phosphorylated JNK expression; and reduced MDA levels, while elevating SOD and GPx activity (P < 0.05). AMPK inhibition by compound C reversed these protective effects. GMC1-irisin combination therapy safeguarded diabetic rats against IR-caused liver damage through suppressing mitochondrial apoptosis by AMPK/JNK signalling, a hopeful therapeutic approach in diabetic patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.