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<p>Acute kidney injury (AKI) causes rapid decline in kidney function and current treatments are expensive and have significant adverse effects. <i>Boerhavia diffusa</i> (Punarnava), an ayurvedic plant has been used as treatment for various diseases. To the best of our knowledge, the effect of Punarnava has never been investigated in TLR4 (toll-like receptor 4)-mediated inflammatory response in cisplatin-induced acute nephrotoxicity. We have studied TLR4 pathway as one mechanism of action of Punarnava and scrutinized the mechanism of action of Punarnava (PUN) on the inflammatory signaling molecules of acute nephrotoxicity. Female BALB/c mice were divided into Control, Cis and Cis + PUN groups. AKI was induced by 15 MPK cisplatin (Cis) on day 0, followed by 500&#xa0;mg/kg of Punarnava. After sacrifice on day 7, the disease parameters were measured. Punarnava treatment restored the clonogenic potential of bone marrow, kidney, spleen, and blood cells. Flow cytometry showed that Punarnava improved the cisplatin-induced anomalies in cellular circulation and migration of immune cells in blood. Additionally, we discovered that Punarnava inhibited the TLR4 pathway. Punarnava acted as a successful TLR4 inhibitor and our research has led to the development of novel treatment strategies based on phytochemistry, which will provide patients with safe options and help lower the incidence of AKI.</p>

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Punarnava (Boerhavia diffusa) Ameliorates Cisplatin Induced Acute Kidney Inflammation by Regulating TLR4 Signaling Pathway in Pre-clinical Mouse Model

  • 期刊论文

  • 发表日期：

    2025年10月21日

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  • Payal Pal,
  • Ena Ray Banerjee

摘要

Acute kidney injury (AKI) causes rapid decline in kidney function and current treatments are expensive and have significant adverse effects. Boerhavia diffusa (Punarnava), an ayurvedic plant has been used as treatment for various diseases. To the best of our knowledge, the effect of Punarnava has never been investigated in TLR4 (toll-like receptor 4)-mediated inflammatory response in cisplatin-induced acute nephrotoxicity. We have studied TLR4 pathway as one mechanism of action of Punarnava and scrutinized the mechanism of action of Punarnava (PUN) on the inflammatory signaling molecules of acute nephrotoxicity. Female BALB/c mice were divided into Control, Cis and Cis + PUN groups. AKI was induced by 15 MPK cisplatin (Cis) on day 0, followed by 500 mg/kg of Punarnava. After sacrifice on day 7, the disease parameters were measured. Punarnava treatment restored the clonogenic potential of bone marrow, kidney, spleen, and blood cells. Flow cytometry showed that Punarnava improved the cisplatin-induced anomalies in cellular circulation and migration of immune cells in blood. Additionally, we discovered that Punarnava inhibited the TLR4 pathway. Punarnava acted as a successful TLR4 inhibitor and our research has led to the development of novel treatment strategies based on phytochemistry, which will provide patients with safe options and help lower the incidence of AKI.