Antinociceptive properties of 25‐methoxy hispidol A, a triterpinoid isolated from Poncirus trifoliata (Rutaceae) through inhibition of NF‐κB signalling in mice

Abstract

The 25-methoxy hispidol A (25-MHA) is a triterpenoid, isolated from the immature fruit of Poncirus trifoliata (Rutaceae). The pretreatment with 25-MHA markedly (p < 0.001) attenuated the formalin-induced biphasic responses as well as acetic acid-induced writhing responses. The intraperitoneal administration of 25-MHA significantly attenuated the mechanical hyperalgesia (p < 0.001) and allodynia (p < 0.05). Similarly, 25-MHA also significantly attenuated (p < 0.001) complete Freund's adjuvant (CFA)-induced paw edema in mice. The 25-MHA treatment significantly attenuated the production of nuclear kappa B (NF-κB) (p65 nuclear subunit). The cytokines are the important mediators of inflammation and pain; however, treatment with 25-MHA exhibited significant inhibition (p < 0.001) on the mRNA expression levels of various inflammatory mediators. The 25-MHA administration also significantly enhanced antioxidant enzymes (p < 0.001) and inhibited the oxidative stress markers. The current study indicates that 25-MHA significantly (p < 0.001) inhibited the nitric oxide (NO) in mice plasma. Similarly, the haematoxylin and eosin (H&E) staining shows that 25-MHA administration significantly inhibited the inflammatory process in the mice paw tissue compared with the CFA-treated group. The 25-MHA treatment did not exhibited any toxicity on the liver, kidney, muscles strength, and motor co-ordination in mice. The 25-MHA was coadministered with the various drugs such as tramadol, piroxicam, and gabapentin to observe the synergistic effect.

Poncirin attenuates CCL4-induced liver injury through inhibition of oxidative stress and inflammatory cytokines in mice

“…During oxidative stress damage the various inflammatory mediators which are released includes IL-1β, IL-6 and TNF-α. These mediators tends to further escalate the liver damage by the feedback mechanism [7][8][9].…”

“…The NO is an important physiological as well as pathological mediators and have been implicated hepatitis. The NO is released during the inflammatory process by the iNOS and its induction is facilitated by the various molecular signaling mechanism such as NF-κB and MAPKs [8,10]. The NF-κB and MAPKs signaling cascades are activated by the upstream signaling molecules such as TIRAF, IRAK and MyD88 [7].…”

ECN from <em>Tussilago Farfara</em> Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Proteins Expression in Surgical Model

“…Thermal hyperalgesia of the plantar surface of the ipsilateral left hind paw was assessed as described previously [46,47]. The temperature of the hot plate was kept at 50 ± 0.5°C.…”

“…The quantitative RT-PCR was used to determine the effect of ECN (10 mg/kg) on the mRNA expression levels of inflammatory mediators (COX-2, iNOS, TNFα, IL-1β and IL-6) and anti-oxidant proteins (Nrf2, HO-1 and NQO1) following 7 and 14 days post PSNL surgery. Trizol Reagent was used to isolate the total RNA from the sciatic nerve and lumbar dorsal spinal cord (L4-L6) tissue of mice as described previously [46,59,60]. Briefly, GenDEPOT 0.2mL 8-strip tubes were used for quantitative PCR.…”

“…NO level in sciatic nerve, lumbar dorsal spinal cord (L4-L6), hippocampus and prefrontal cortex tissues of day 7, 10 and 14 post PSNL surgery were determined by Griess assay according to the method previously described [46,63]. The concentration of NO was determined by using Griess reagent, 1% sulfanilamide and 2.5% phosphoric acid.…”