Table 3 Effect of Nigella sativa and thymoquinone on inflammation

Cingi et al. 2011 [46]

Intranasal platelet activating factor-induced rhinosinusitis model in Sprague-Dawley rats.

80 mg/kg oral TQ.

1. Degree of vascular congestion

2. Intensity of inflammatory cell infiltration

3. Degree of epithelial injury

Treatment with TQ reverses the intranasal platelet activating facto-induced histological changes.

TQ have been shown to be beneficial for the resolution of rhinosinusitis.

Demirel et al. 2018 [36]

Bacterial infection-induced otitis model in Wistar rats.

0.1 and 0.4% topical TQ.

1. Histopathological assessment.

2. Bacterial assessment.

Treatment of TQ reverses infection-induced histopathological changes and reduces bacterial growth in the ear canal.

TQ shows bacteria eradication and anti-inflammatory properties

Sezen et al. 2018 [39]

Cardiac ischemia-induced lung injury in Wistar rats

25 mg/kg TQ.

1. Apoptotic markers in the lung.

2. Histological assessment.

Treatment of TQ reverses cardiac ischemia-induced histopathology changes via suppression of apoptosis.

TQ protects against lung injury via inhibition of apoptosis.

El-Ebiary et al. 2016 [33]

Cadmium chloride (CdCl₂)-induced lung damage in Wistar rats

1 ml/kg oral NSO.

1. Histopathological assessment.

2. Scanning electron microscopy.

Treatment of NSO reverses histopathological changes induced by CdCl₂ with normal pneumocytes morphology and intra-alveolar septum thickness.

Treatment with NSO ameliorated pathological changes in CdCl₂ poisoned rats.

Su et al. 2016 [43]

Ovalbumin-induced asthma in Balb/C mice.

3 mg/kg oral TQ.

1. Cytokines level.

2. Fibrotic markers.

3. Histopathological assessment.

4. Angiogenic factors.

5. HUVEC tube formation.

6. Protein kinase activity.

Treatment of TQ reverses histopathology changes of asthma induced by ovalbumin via suppression of inflammation and angiogenesis.

TQ have anti-inflammatory and anti-angiogenesis properties in ovalbumin-induced asthmatic mice.

Al-Trad et al. 2016 [47]

Streptozotocin (STZ)-induced nephropathy in diabetic rats.

50 mg/kg oral TQ and 2 ml/kg oral NSO.

1. Renal pathology parameters.

2. Expression of Podocin.

3. Fibrotic markers.

4. Angiogenic marker.

Both TQ and NSO treatment demonstrated comparable reversal of diabetic-induced renal pathology via expression of podocin and inhibition of fibrosis and angiogenesis.

TQ & NSO improves pathological changes in diabetic-induced nephropathy.

Omran 2013 [45]

Nephropathy in STZ-induced diabetic rats.

50 mg/kg oral TQ.

1. Renal pathology parameters.

2. Histopathological assessment.

3. Epithelial markers.

4. Mesenchymal markers.

Treatment of TQ reverses the diabetic-induced renal histopathological changes via inhibition of the epithelial to mesenchymal transition.

TQ improves renal functions via inhibition of epithelial to mesenchymal transition in diabetic nephropathy.

Hammad & Lubbad 2016 [41]

Reperfusion therapy-induced nephropathy in male Wistar rats.

10 mg/kg oral TQ.

1. Renal pathology parameters.

2. Cytokine levels.

Treatment of TQ resulted reversal of reperfusion therapy-induced histopathological changes via the inhibition of inflammation.

TQ improves renal functions via inhibition of inflammation following reperfusion therapy-induced nephropathy.

Yang et al. 2016 [44]

Ethanol (EtOH)-induced liver injury in C57/BL6 mice.

20 mg/kg or 40 mg/kg oral TQ.

1. Liver pathology parameters.

2. Histopathological assessment.

3. Expression level of SIRT1, LKB1 and AMPK.

Treatment of TQ reverses the EtOH-induced liver pathological changes via upregulation of SIRT1, LKB1, and AMPK.

TQ regulates LKB1 and AMPK signalling that is associated with inflammation in ethanol-induced liver injury.

Mabrouk 2018 [37]

Lead (Pb)-induced testicular damage in Wistar rats.

5 mg/kg/day oral TQ.

1. Testicular pathology parameters.

2. Histopathological assessment.

Treatment of TQ reverses the Pb-induced testicular pathological.

TQ have protective effect against Pb-induced testicular damage.