Lactobacillus rhamnosus GKLC1 ameliorates cisplatin-induced chronic nephrotoxicity by inhibiting cell inflammation and apoptosis

Sustained usage of the chemotherapeutic drug cisplatin may lead to chronic kidney disease (CKD). Despite cisplatin being toxic to the kidneys, the efficiency of its therapeutic effects cannot be completely replaced with other drugs. Probiotics can produce various strain-specific health-promoting effects and suppress many specific diseases. In this study, we present the alleviation of cisplatin-induced CKD with a probiotic, Lactobacillus rhamnosus GKLC1. Intermittent low doses of cisplatin were given to male CB57BL/6 mice (n = 6), which induced CKD symptoms such as weight loss, lesions in kidney tissue, and increases in blood urea nitrogen (BUN) and creatinine (CRE) in serum. The rats received two weeks of L. rhamnosus GKLC1 orally at doses of 125, 250, and 500 mg/kg B.W./day. After the treatment, significant dose-dependent reductions were observed in the kidney index, histopathological scoring, serum BUN, and CRE. An LLC-PK1 kidney cell assay revealed that L. rhamnosus GKLC1 suppressed the nephrotoxicity of cisplatin by reducing the inflammation via the MAPKs/NF-ĸB/COX-2 pathway, inhibiting apoptosis via the p53/Bax/Caspase-3 pathway, and ameliorating fibrosis via the STAT3 pathway. We conclude that L. rhamnosus GKLC1 could be applied as an agent to ameliorate the development of CKD. Probiotics L. rhamnosus GKLC1 significantly reduced blood urea nitrogen (BUN) and creatinine (CRE) in cisplatin-induced chronic kidney disease (CKD) mice. The kidney cell assay revealed that probiotics GKLC1 protected kidney by inhibiting inflammation via Akt/NF-ĸB/COX2 pathway, apoptosis via p53/Bax/Caspase-3 pathway, and fibrosis via STAT3 pathway. [Display omitted] •Probiotics GKLC1 reduced serum BUN and CRE in cisplatin-induced CKD mice.•Anti-inflammation effects were revealed in the probiotic group in CKD model.•The MAPKs expressions were inhibited by fermented supernatant from GKLC1.•Strain GKLC1 protected kidney via regulating p53/Bax/Caspase-3 pathway.•GKLC1 could act as an anti-fibrotic agent.