Aqueous leaves extract of Madhuca longifolia attenuate diclofenac‐induced hepatotoxicity: Impact on oxidative stress, inflammation, and cytokines

Abstract

Diclofenac is a Non-Steroidal Anti-inflammatory drug which is used as an analgesic. It is known to cause heptotoxicity on over dose and long term usage. Madhuca longifolia is an evergreen tree found widely in India that is known to have several ethnomedical uses. The aim of our study is to evaluate the beneficial effect of the aqueous leaf extract of M. longifolia against diclofenac-induced toxicity. Rats were dived into five groups of six rats each. Group-I was normal control. Group-II was administered with diclofenac (50 mg/kg. b.w./day, i.p) on 4th and 5th day. Group-III rats were treated with aqueous leaf extract of M. longifolia (500 mg/kg b.w./day, oral) for 5 consecutive days and diclofenac (50 mg/kg. b.w./day, i.p) was given on 4th and 5th day. Silymarin (25 mg/kg. b.w./day, oral) was used as standard drug which was given to the rats of group-IV along with diclofenac on 4th and 5th day. Aqueous leaf extract of M. longifolia (500 mg/kg b.w./day, oral) alone was administered in group-V. After the study period, the rats were evaluated for liver enzyme markers, antioxidant parameters, histopathological changes, and cytokines levels. The hepatic proinflammatory mediator cytokines like TNF-α, IL-6, and IL-1β were evaluated through ELISA. The protein expression of Caspase-3, COX-2, and NF-κB were analysed through Western blotting techniques. Aqueous leaves extract of M. longifolia was able to normalize the changes caused by diclofenac. Current study indicatesthe protective effect of the aqueous leaves extract of M. longifolia against diclofenac-induced toxicity.

Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response

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Selenium attenuates diclofenac‐induced testicular and epididymal toxicity in rats

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Tubuloside A, a phenylethanoid glycoside, alleviates diclofenac induced hepato‐nephro oxidative injury via Nrf2/HO‐1

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