Browsing by Author "Singh, L"

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    Amla (Emblica officinalis) alleviates doxorubicin-induced cardiotoxicity and nephrotoxicity in rats
    (2024-11) Arora, M; Singh, M; Tomar, R; Singh, L; Jangra, A
    Introduction: Doxorubicin (DOX) is a widely used anticancer drug known for its significant cardiotoxic and nephrotoxic effects. Seeking remedies to mitigate these adverse effects is crucial. This study investigates the potential of Emblica officinalis (Amla) extract, a prominent component in Chinese and Indian traditional medicine systems, in alleviating DOX-induced cardiotoxicity and nephrotoxicity. Methods: DOX (20 mg/kg i.p., once) was given to rats to cause acute cardiotoxicity and nephrotoxicity. Rats received 16 similar and cumulative doses of DOX (1.25 mg/kg, i.p.) on alternate days for chronic cardiotoxicity and nephrotoxicity. Biochemical and histological evaluations were done to confirm the onset of cardiotoxicity and nephrotoxicity. Results: The cardioprotective and nephroprotective effects of Amla extract (AE) (150 mg/kg p.o. and 300 mg/kg p.o) were evaluated in comparison to Vitamin E (25 mg/kg p.o.). The treatment with AE (300 mg/kg/day, p.o.) considerably prevented DOX-induced cardiotoxicity, nephrotoxicity, and oxidative stress by positively altering the integrity of glomeruli, restoring the tissue GSH and decreasing serum TBARS. AE (300 mg/kg) was found to be more cardioprotective and nephroprotective than Vitamin E (25 mg/kg p.o.). Discussion: It may be concluded that the induction of cardiotoxicity and nephrotoxicity in rats may be due to DOX-induced oxidative stress, and chronic treatment with AE (300 mg/kg) is an effective way to alleviate the cardiotoxic and nephrotoxic adverse effects of DOX in rats. Moreover, given Amla’s historical and contemporary significance in Chinese and Indian traditional medicine systems, its potential therapeutic role merits further exploration in clinical settings.
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    Hypoxia induced lactate acidosis modulates tumor microenvironment and lipid reprogramming to sustain the cancer cell survival
    (2023-01) Singh, L; Nair, L; Kumar, D
    It is well known that solid hypoxic tumour cells oxidise glucose through glycolysis, and the end product of this pathway is fermented into lactate which accumulates in the tumour microenvironment (TME). Initially, it was proclaimed that cancer cells cannot use lactate; therefore, they dump it into the TME and subsequently augment the acidity of the tumour milieu. Furthermore, the TME acts as a lactate sink with stope variable amount of lactate in different pathophysiological condition. Regardless of the amount of lactate pumped out within TME, it disappears immediately which still remains an unresolved puzzle. Recent findings have paved pathway in exploring the main role of lactate acidosis in TME. Cancer cells utilise lactate in the de novo fatty acid synthesis pathway to initiate angiogenesis and invasiveness, and lactate also plays a crucial role in the suppression of immunity. Furthermore, lactate re-programme the lipid biosynthetic pathway to develop a metabolic symbiosis in normoxic, moderately hypoxic and severely hypoxic cancer cells. For instance: severely hypoxic cancer cells enable to synthesizing poly unsaturated fatty acids (PUFA) in oxygen scarcity secretes excess of lactate in TME. Lactate from TME is taken up by the normoxic cancer cells whereas it is converted back to PUFAs after a sequence of reactions and then liberated in the TME to be utilized in the severely hypoxic cancer cells. Although much is known about the role of lactate in these biological processes, the exact molecular pathways that are involved remain unclear. This review attempts to understand the molecular pathways exploited by lactate to initiate angiogenesis, invasiveness, suppression of immunity and cause re-programming of lipid synthesis. This review will help the researchers to develop proper understanding of lactate associated bimodal regulations of TME.