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Osteoarthritis (OA) represents the highest degenerative disorder. Because cartilage erosion is a common pathological alteration in OA, targeting some key metalloproteinases such as MMP-3, ADAMTS-5 besides their inhibitor TIMP-3 by natural products, could be an effective strategy to protect against osteoarthritis. Forty female Wister rats were categorized into five equal groups. Control, osteoarthritic (OA) (monosodium iodoacetate (MIA) 2 mg/50 µL saline, single intra-articular injection), OA+ indomethacin (2 mg/kg/daily/orally), OA+ nano-naringenin (25 mg/kg/daily/orally), and OA+ Amphora coffeaeformis (772 mg/kg/daily/orally). Treatments were initiated on the 8th day after osteoarthritis induction and continued for 28 days thereafter. Finally, blood and knee joint samples were collected from all rats for biochemical and histopathological evaluations. The current study showed that MIA induced oxidative stress, which resulted in changes in the inflammatory joint markers associated with increased right knee diameter and higher clinical scores for lameness. Amphora coffeaeformis followed by nano-naringenin exhibited a potential anti-arthritic activity by reducing the concentrations of serum MMP-3, ADAMTS-5, and joint MDA and increasing the levels of serum TIMP-3 and joint GSH, similar to indomethacin. The histopathological results confirmed these outcomes. In conclusion, Amphora coffeaeformis and nano-naringenin can be considered as natural therapeutic agents for osteoarthritis owing to their antioxidant and anti-inflammatory activities.

Concurrent administration of drugs may alter their pharmacokinetic parameters, so; investigation to what extent bromhexine hydrochloride affects the pharmacokinetic behavior of tilmicosin was our aim of this work. Ten broiler chickens were classified into two groups as follow, the first one (tilmicosin group) was given single oral dose of tilmicosin (20 mg/kg.b.wt.) while the 2nd (pre-treated group) was given single oral dose of bromhexine hydrochloride (1 mg/kg.b.wt.) followed by single oral dose of tilmicosin (20 mg/kg.b.wt.) one hour later. The serum concentration of tilmicosin was measured using High Pressure Liquid Chromatography (HPLC) method. The results revealed that the mean serum concentrations of tilmicosin were significantly lower in pre-treated group when compared with tilmicosin alone group at the corresponding time intervals. Pharmacokinetic parameters were significantly differed (p<0.001) between both groups. The maximum serum concentration were (Cmax0.70±0.02, 0.81±0.04µg/ml), achieved at Tmax of (tmax 0.89±0.16, and 2.10±0.06h), absorption half-life (t0.5ab) of 0.16±0.08, and 0.37±0.01 hour, area under curve (AUC) of 12.96±0.42 and 16.73±0.42µg.h/ml) in tilmicosin-bromhexine and tilmicosin alone groups respectively. In conclusion, based on the obtained pharmacokinetic parameters, these findings showed that bromhexine accelerates the tilmicosin penetration into body tissues, achieving higher and faster concentrations than when given tilmicosin alone.

Sesame oil has been exhibited to have anti-in ammatory and antioxidant in uences. The goal of this experiment was to look into sesame oil's hepato-protective properties and underlying processes in valproic acid-induced hepatotoxicity. Molecular docking was carried out to clarify the functional and structural underlying mechanism of sesame oil ameliorative effect. Mice were given 8 ml/kg/day of sesame oil (orally) and 100 mg/kg/day of valproic acid (i.p.) for 21 days. The results revealed that valproic acid caused a considerable increase in hepatic malondialdehyde (MDA) levels while decreasing the activity of glutathione peroxidase (GPx) enzyme. There was also a signi cant rise in serum levels of interleukines 1β & 6 (IL-1β & IL-6) and a signi cant decrease in hepatic (PXR) gene expression level.Sesame oil co-administration with valproic acid signi cantly normalized the antioxidant and antiin ammatory status and upregulated the gene expression level of PXR. In silico docking analysis results con rmed these results. This study concluded that supplementation of sesame oil attenuated valproic acid induced oxidative stress and in ammation. Hence, it was recommended as a dietary supplement for protection against valproic acid induced hepatotoxicity.

Background Cisplatin is a wide-ranging antineoplastic drug. Neurotoxicity is one of cisplatin’s side effects that restrict its usage. This study aimed to investigate the possible protective properties of sweet basil oil against cisplatin-induced neurotoxicity in mice. A docking study was carried out to elucidate the fundamental mechanism of sweet basil oil’s ameliorative influence. Thirty male mice were allocated into three groups as follows: control group, cisplatin group (2.3 mg/kg), and sweet basil oil group (25 µl/kg basil oil + cisplatin 2.3 mg/kg). Cisplatin was given for five successive days, followed by five days of rest, for two cycles, while sweet basil oil was orally administered for 21 successive days. Results Our results revealed that sweet basil oil’s antioxidant activity ameliorated the oxidative stress induced by cisplatin in mice’s brains via lowering MDA levels and increasing CAT activity and Nrf2 levels. Also, the anti-apoptotic activity of sweet basil oil was obvious via lowering the gene expression levels of Bid and caspase-3 but did not affect the serum level of P38 MAPK. Changes in acetylcholinesterase activity, serotonin and dopamine levels induced by cisplatin were significantly alleviated by sweet basil oil. Conclusion Sweet basil oil can be used as a food supplement to guard against cisplatin-induced neurotoxicity. Graphical abstract

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Gibberellic acid (GA3) is a well-known plant growth regulator used in several countries, but its widespread use has negative effects on both animal and human health. The current study assesses the protective effect of royal jelly (RJ) and Chlorella vulgaris (CV) on the genotoxicity and hepatic injury induced by GA3 in rats. Daily oral administration of 55 mg/kg GA3 to rats for 6 constitutive weeks induced biochemical and histopathological changes in the liver via oxidative stress and inflammation. Co-administration of 300 mg/kg RJ or 500 mg/kg CV with GA3 considerably ameliorated the serum levels of AST (aspartate aminotransferase), ALT (alanine aminotransferase), ALP (alkaline phosphatase), γGT (gamma-glutamyl transferase), total bilirubin, and albumin. Lowered malondialdehyde, tumor necrosis factor α (TNF-α), and nuclear factor κB (NF-κB) levels along with elevated SOD (superoxide dismutase), CAT (catalase), and GPx (glutathione peroxidase) enzyme activities indicated the antioxidant and anti-inflammatory properties of both RJ and CV. Also, they improved the histological structure and reduced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions along with up-regulating peroxisome proliferator activated receptor α (PPARα) and down-regulating activator protein 1 (AP-1) gene expression. Additionally, chromosomal abnormalities and mitotic index were nearly normalized after treatment with RJ and CV. In conclusion, RJ and CV can protect against GA3-induced genotoxicity and liver toxicity by diminishing oxidative stress and inflammation, and modulating the PPARα/AP-1 signaling pathway.

D oxorubicin is an anthracycline antibiotic. It is also known as adriamycin. Doxorubicin is commonly used in the chemotherapy of breast cancer, lung cancer, leukemia and solid tumors (Xinyong et al., 2020). This cardiotoxicity has serious implications, resulting in a bad prognosis and deaths for up to 61% of patients (Wouters et al., 2005).Previous studies stated that the doxorubicin induced cardiac toxicity involves generation of huge amounts of reactive oxygen and reactive nitrogen species (ROS and RNS) which can obviously cause cardiac toxicity (Gilliam and research Article Abstract | Doxorubicin is a chemotherapeutic drug broadly used for the treatment of a wide range of malignancies.Many studies have shown that natural compounds derived from plants have medicinal and antioxidant properties. The purpose of the current investigation was to investigate if almond oil could protect male mice against doxorubicininduced cardiotoxicity. The experimental mice were divided into three groups; control group: received 0.9 percent saline, doxorubicin group: Mice were intraperitoneal injected with doxorubicin (5 mg/kg) ithree times over a period of two weeks (dose every five days) and almond oil group: Mice were administered almond oil orally (2.26 g/kg) using oral gavage daily over a period of three weeks, one week prior to the doxorubicin injection and two weeks along with doxorubicin injection. The effects and mechanisms of doxorubicin on superoxide dismutase activities were elucidated by molecular docking studies. Treatment with almond oil attenuated lipid peroxidation, improved superoxide dismutase (SOD) activities that are associated with doxorubicin administration. Also almond oil considerably modulated the gene expression of toll like receptor 4 (TLR4) and lowers the serum levels of both nuclear factor κB (NF-κB) and tumor necrosis factor α (TNF-α). The elevated levels of Creatine Kinase -MB (CK-MB), Lactate Dehydrogenase (LDH), and Troponin-1 induced by doxorubicin injection were neutralized by almond oil supplementation. Almond oil ameliorated all the histological alterations caused by doxorubicin. The administration of almond oil with doxorubicin modulated the doxorubicin-induced changes in serum and cardiac tissue in mice due to its anti-inflammatory and antioxidant properties.